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Kidney Disease > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

Major functions of Kidneys?

A

Excretion of wastes/toxic products (nitrogen containing materials)
Fluid balance (excrete urine)
Electrolyte balance (Na+, K+, and Ca2+)
Acid base balance  pH  Mainly maintained by production of bicarb in the kidneys
Calcium homeostasis  Due to endocrine functions
Regulation of RBC production  Due to endocrine function of erythropoiten

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2
Q

CKD Definition

A

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

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3
Q

ESRD is defined as…. Tx includes

A

Defined as GFR < 15 mL/min
Need dialysis or kidney transplant to live

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4
Q

Risk factors for CKD

A

Diabetes
High blood pressure
Heart and blood vessel (cardiovascular) disease
Obesity
Family history of kidney disease
Abnormal kidney structure
Older age
Smoking

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5
Q

Signs and symptoms develop over…..

A

time if kidney damage progresses slowly

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6
Q

Can CKD be diagnosed without signs of kidney damage? What would be used for diagnosis? If so, when?

A

YES

GFR <60ml/min for atleast 3 months

No kidney damage –> NO proteinuria

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7
Q

Can CKD be diagnosed if GFR is > 60 ml/min? If so, when?

A

YES

  • evidence of kidney damage
  • if proteinuria is present for 3 months
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8
Q

G1 and G2 symptoms and tx

A

No symptoms

Identify cause and reverse it. Monitor albumin and GFR.

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9
Q

G3 a sx and tx

A

No symptoms
- Monitor albumin and GFR, blood pressure, general health
Try to slow down progression

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10
Q

G3 b Sx and Tx

A

Early smyptoms may appear –> tiredness, poor appetite and itching
- Same as before; however, learn more about CKD tx options

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11
Q

G4 Sx and Tx

A

Sx: Tiredness, poor appetite, and itching may get worse
- Same as before; however, plan for tx: dialysis acess, transplant asses, or info on non-dialysis supportive care

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12
Q

G5 Sx and tx

A

Sx: Severe fatigue, nauseau, difficulty breathing, and itchiness

Same as before: however, continue with non-dialysis supportive care, plan for transplant, or strat dialysis

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13
Q

In what stages is CKD asymptomatic?

A

Stages 1 and 2

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14
Q

Does GFR decrease with age? If so, how much?

A

GFR declines with age starting after 20
1 mL/min/year in healthy people

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15
Q

Progression of CKD depends on….

A

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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16
Q

Is CKD reversible? Why?

A

No –> nephrons are lost

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17
Q

Why is CKD bad on nephrons?

A

Remaining nephrons take on more filtrate to accommodate
This “hyperfiltration” effect is also damaging the remaining nephrons

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18
Q

How much % of nephrons can be lost without clinical symptoms?

A

50%

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19
Q

When does azotemia occur?

A
  • Loss of 80% of nephrons
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20
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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21
Q

In CKD and AKI, a serious complication is…. and is caused by….

A

Although Cr and urea are clearly elevated in CKD, the “uremic syndrome (uremia)” is caused by numerous toxins
Uremia is a serious complication of both CKD and AKI
Hundreds of toxins have been implicated

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22
Q

Na+ balance in CKD manifestation….

A

Healthy kidneys will adjust Na and water excretion based on intake
In CKD, adjustment is often lost so intake exceeds excretion
Results in Na retention and extracellular fluid volume (ECFV) expansion (Edema and/or HTN)

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23
Q

The progression of fluid symptoms occurs….. and can cause….

A

Initially, asymptomatic  Slowly progressive
Eventually, can become very difficult to manage, contributing to heart failure, hypertension, edema and weight gain (due to the build up of fluid due to swelling)

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24
Q

Are diuretics useful in CKD? When do they lose effectiveness?

A

Reduce blood pressure and treat swelling (edema)
Thiazide diuretics often lose effectiveness when GFR decreases below 30 mL/min

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25
Q

Which diuretics are preffered in CKD? Dose?

A

Loop diuretics (furosemide) preferred but higher doses (compared to healthy people) are often needed

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26
Q

In diuretic resistance, what is used?

A

loop diuretic + thiazide diuretic (metolazone) may be combined

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27
Q

When is dialysis required in regards to diuretic usage?

A

Untreatable edema and HTN will require dialysis

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28
Q

ESRD Definition

A

Kidneys permanently fail to work

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29
Q

Diagnosis Tests of ESRD

A

Blood tests – blood cell counts, electrolyte levels, and kidney function
Urine tests
Sonography (renal ultrasound)
Kidney biopsy (renal needle biopsy)
CT scan

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30
Q

Tx options for for ESRD

A

Dialysis – not cure
Peritoneal dialysis
Hemodialysis

Kidney transplantation

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31
Q

In regards to transplanttaion, it is best when…. Why?

A

Pre-emptive kidney transplant

Transplantation before reaching ESRD
Lower risk of rejection, improved survival rates, improved quality of life, lower treatment costs, and avoidance of dialysis

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32
Q

Hypertension and CKD

A

Increased glomerular pressure (pushing the blood through the glomerulus)  Kidney has to work harder –> Hypertrophy  pressure causes damage of the nephrons  No longer like AKI, progression is slow

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33
Q

Chronic Glomerular Hypertension can cause…

A

hypertrophy of tissues and loss of nephrons altogether

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34
Q

____ can cause remodelling over time

A
  • Elevated angiotensin II
35
Q

Elevated angiotensin II can cause

A
  • remodelling over time
36
Q

Glomerular dysfunction leads to…. which….

A

protein leakage accelerates damage

37
Q

First Line Tx of Hypertension and CKD. What should accompany these drugs?

A

ACEi
ARBs

(along with diuretics depending on volume)

  • Salt restriction should accompany drugs
38
Q

How can proteinuria cause CKD?

A
  • Direct cellular damage

Proteins are toxic to tubular cells –> Increased production of inflammatory cytokines –> Immune response

  • Damage leads to scarring, structural change and progressive loss of renal function
39
Q

What is the number 1 cause of ESRD?

A
  • Diabetes
40
Q

Diabetes causes CKD by….

A
  • Glomerular messangial matrix expansion and renal vascular damage
  • Glycated products (sugar coated molecules) somehow damage kidney structures directly
41
Q

Why is glucose control so important in people with diabetes?

A

Slowing the progression to CKD is one of the main benefits of glucose control in people with diabetes

42
Q

Diabetes causes changes in….such as…..

A
  • Glomerulus Structural and morphological changes
  • Change in capillary loops
  • More messangial cells (res[responsible for structure of capillary loops and regulate filtrataion rate)
  • Podocytes no longer exist (slits for filtratiopn)
  • Thicker basemnt mebrane
  • Fil;tration barrier gonr
43
Q

Classic risk factors of CVD?

A

HTN, lipid, sympathetic nervous system tone)

  • CKD pt’s have these risk factors
44
Q

Non-traditional risk of artherosclerosis appear to…. risk of ACVD such as

A

Accelerate

Anemia
High phosphate, high parathyroid hormone (PTH)
Generalized inflammation

45
Q

Heart failure is exacerbated by….

A

issues with high volume

46
Q

ACEi and ARBS are most benficial to…

A

people with more severe disease

47
Q

ACEi and ARB’s are first line for…

A

patients with diabetes + nephropathy (CKD pt’s)

48
Q

As tubules lost, which electrolyte becomes problematic to excrete?

A

K+

49
Q

When does hyperkalmeia become a serious problem?

A

When GFR falls below 5 mL/min

50
Q

Hyperkalemia Tx?

A

K-wasting diuretics (Thiazide, and Loop Diuretics)
Minimization of K-sparing medications
Potassium-binding resins (no digestion in stomach)
Sodium polystyrene sulfonate (Kayexalate)
Calcium polystyrene sulfonate (Calcium Resonium)

51
Q

Sodium Polyseterene Sulfonate MOA

A
  • Bind K+ in G.I. (in exchange for Na+)
52
Q

Sodium Polyseterene Sulfonate A.E.

A
  • Watch for effects of increased Na+ (may cause retention of fluid and ECF volume increase)
53
Q

Sodium Polyseterene Sulfonate Onset of ACtion

A
  • Slow (days)
  • Should not be used as an emergency treatment for life-threatening hyperkalemia
54
Q

Calcium polystyrene sulfonate and Sodium Polyseterene Sulfonate D.I. and cautions

A

Will interfere with other drug absorption. You have to leave time in between to prevent interference with absorption

Cannot use this in emergency situations  Slow onset

55
Q

Metabolic Acidosis –> Equation of regulation of pH

A

H+ + HCO3- <—> H2CO3 <–> CO2 + H2O

56
Q

What enzzyme is responsible for bicarbonate production?

A

Carbonic Annhydrase

57
Q

The kidneys maintain bicarbonate concnetration by….

A

-CO2 can be taken up by renal tubule and be converted to HCO3
- HCO3 re-absorbed into the blood

58
Q

HCO3 is reabsorbed where? How much?

A
  • 85-95% of bicarb is reabsorped at proximal tubule
59
Q

Non-fixed Acid in the body is due to….

A

CO2

60
Q

Production of CO2 in the body is… as a result of…

A

Normal
- TCA cycle, ATP generation

61
Q

respiratory acidosis occurs in… as a result of

A

In lung diseases, CO2 retention

62
Q

Volatile Acid Example and Elimination

A

CO2 –> respiration

63
Q

Fixed acids Examples

A
  • Not by respiratory system
  • Lactic acid –> Exercise –> Anareaobic Glycolysis
  • Ketones –> Fatty acid degredation
64
Q

How are fixed acids eliminated? How does the kidney excrete H+?

A

Renally

Secretion of H+ ions
Secreted into lumen directly (excrete directly in urine)
Combines with NH3 already circulating (highly soluble and excreted)

Secretion of NH4+ ions
Within tubular cells and secretion into tubular lumen

65
Q

What is the mian nitrogen molecule excreted from the body?

A

Urea

66
Q

Urea Mechanism of Excretion

A

Circulating NH3 molecules are combined with CO2 in the liver to form urea
Urea is odorless and colourless and highly soluble in water
Easily excreted by the kidney

67
Q

Metabolic Acidosis

A

Study Chart

68
Q

When does metabolic acidosis occur? (GFR)

A

GFR < 20 mL/min

69
Q

Tx of metabolic acidosis

A

Sodium bicarbonate can be used to manage (when bicarbonate levels fall

70
Q

Calcium homeostasis kidney mechanism

A

Kidney plays a role in calcium homeostasis through its role in the activation of vitamin D
In addition to low serum calcium, the kidney fails to excrete phosphate

71
Q

Management of Calcium/Phosphate in CKD

A

Decrease phosphorus in diet
Phosphate binding agents such as Sevelamer
Calcitriol (1,25-dihydroxyvitamin D)

72
Q

In CKD Ca2+ levels are

A

LOW

73
Q

How does the body respond to low Ca2+?

A

Parathyroid gland senses the level of ionized calcium in the blood
If Ca2+ falls, the gland secretes parathyroid hormone (PTH)

PTH effects

Kidney
Promotes renal tubular calcium reabsorption
Promotes phosphate excretion
Stimulates production of 1,25-dihydroxyvitamin D (active Vitamin D)
Bone
Promotes catabolism of bone to release calcium and phosphorus into bloodstream

74
Q

Vitamin D products in canada

A

Alfacalcidiol
Calcitriol
Cholecalciferol
Ergocalciferol

75
Q

Alfacalcidiol

A

Requires conversion to calcitriol in the liver

76
Q

Calcitriol

A

Active

77
Q

Cholecalcifriol

A

Synthesized in skin
Found in fatty fish, fish oils, etc
Still requires 2-step activation (liver and kidney)

78
Q

Ergocalciferol

A

Occurs in nature - found in wild mushrooms
Similar to vitamin D3 (above), requires 2 step activation (liver and kidney)

79
Q

How do kidneys regulate RBC production?

A

Kidneys contain specialized cells that detect low oxygen levels in the blood

Hypoxia-induced erythropoietin (EPO) production
Act as a critmeter to maintain hematocrit

80
Q

What hormone is important for RBC production?

A

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

81
Q

Anemia can occur when… (GFR)

A

GFR falls below 30-45 mL/min (Level 3b)

82
Q

Anemia in CKD tx

A

Iron supplementation (boost the function of hemoglobin)

Oral and IV products considered
Erythropoiesis-stimulating agents (EPO replacement)

Epoetin alfa (Eprex®) – Recombinant EPO with same amino acid sequence
Darbepoetin alfa (Aranesp®) – Amino acids modified for longer duration of action

83
Q

Why is monitoring required for anemia tx?

A

Monitoring of therapy requires close attention to hemoglobin level
Increasing RBC production can result in adverse effects such as hypertension or thrombosis (i.e., clotting)

84
Q

At what GFR does ADR risk increase? What do we do?

A

Approximately half of patients with GFR < 60 mL/min are at risk for ADRs

Adjust dose

Kidney Disease (3 decks)

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