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Nursing Semester 2 > Monica - Exam 4: Chronic Kidney Disease > Flashcards

Monica - Exam 4: Chronic Kidney Disease Flashcards

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1
Q

What are the three basic functions of the kidneys?

A
  1. regulatory
  2. excretory
  3. endocrine
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2
Q

The kidneys regulate:

A
  1. blood pressure via RAAS
  2. fluid and electrolyte balance
  3. acid-base balance
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3
Q

The kidneys excrete:

A

waste products: metabolic waste, toxins, excess water, creatine

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4
Q

Endocrine functions of the kidneys:

A
  1. erythropoietin
  2. renin
  3. calcitriol
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5
Q

erythropoietin

A

hormone released by the kidneys when oxygen levels are low in order to stimulate the production of RBCs in bone marrow

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6
Q

chronic kidney disease

A
  • irreversible, progressive
  • develops over months to years
  • unable to: excrete waste products, respond to acid-base imbalance, control BP and fluid voume
  • progresses to end-stage renal disease requiring dialysis or kidney transplant
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7
Q

non-modifiable risk factors

A
  • family hx of kidney disease, DM, HTN, CVD
  • older than 60
  • ethnicity: african-american (2.7x higher r/t HTN), hispanics (1.5x higher)
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8
Q

modifiable risk factors

A

HTN, DM

**two most common causes of CKD

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9
Q

diabetic nephropathy

A

increased permeability of protein

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10
Q

microabuminuria

A

small amounts of protein in urine

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11
Q

diabetic nephropathy

A

increased permeability of protein

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12
Q

microalbuminuria vs. proteinuria

A

small amounts of protein in urine vs. larger amounts of protein in urine

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13
Q

How is the diagnosis of diabetic nephropathy confirmed?

A

by proteinuria on at least 2 occasions 3-6 mos. apart

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14
Q

How does HTN increase the risk of CKD?

A
  • kidney arteries narrow, weaken, and harden leading to impaired blood flow
  • gradual deterioration of glomerulus
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15
Q

HTN is both a ____ and ____ of CKD.

A

cause and consequence

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16
Q

How does DM increase the risk of CKD?

A
  • damage to glomerular capillaries

- they become hyperpermeable allowing protein to pass through

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17
Q

Which renoprotective drugs are indicated to manage HTN and DM?

A

ACE inhibitors and ARBs - to protect against further damage to kidneys

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18
Q

Which lab values are indicators of kidney function?

A

BUN + Cr, GFR

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19
Q

BUN

A

blood urea nitrogen - protein broken down by the liver and excreted in urine so indicator liver AND kidney function

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20
Q

Creatinine

A

waste-product of muscle metabolism

*specific to kidney function

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21
Q

GFR: normal range

A

90 - 120 mL/min

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22
Q

What is GFR a measure of?

A

the amount of blood filtered through the glomerulus per minute

  • indicates the ability of the glomerulus to filter wastes and the progression of CKD
  • *best indicator of kidney function
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23
Q

African-Americans have a ______ GFR than other races. Why?

A

HIGHER GFR. d/t a greater average muscle mass that either generates more creatine or eliminates less creatinine…?

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24
Q

stage 1 CKD: GFR

A

> = 90 - kidney damage with normal GFR

25
Q

Stage 1 CKD: clinical action and symptoms

A
  • diagnosis and slowing of progression by treating modifiable risk factors (HTN, DM)
  • renoprotective anti-hypertensives, lifestyle modifications
  • pts often asymptomatic
26
Q

Stage 2 CKD: GFR

A

60 - 89 - kidney damage with mildly decreased GFR

27
Q

Stage 2 CKD: clinical action and symptoms

A
  • estimating progression (via GFR)

- pts often asymptomatic

28
Q

Stage 3 CKD: GFR

A

30 - 59 - moderately decreased GFR

29
Q

Stage 3 CKD: clinical action and symptoms

A
  • evaluating and treating complications

- progressive clinical and lab complications

30
Q

Stage 4 CKD: GFR

A

15 - 29 - severely decreased GFR

31
Q

Stage 4 CKD: clinical action and symptoms

A
  • dialysis, kidney transplant

- progressive clinical and lab complications

32
Q

Stage 5 CKD: GFR

A

< 15 - kidney failure

33
Q

Stage 5 CKD: clinical action and systems

A
  • replacement (if uremia is present)

- usually prominent uremia symptoms

34
Q

creatinine clearance

A

total amount of creatinine in urine

  • decreased = decreased GFR and renal impairment
  • used to evaluate kidney function
35
Q

24 hour urine collection

A
  • captures maximal excretion of substance
  • evaluation of daily kidney function
  • creatinine, proteins, electrolytes, toxins excreted over a 24 hour period
36
Q

The collection process for 24 hour urine:

A
  • discard first void
  • write start time on container
  • end time 24 hours after
  • keep container on ice
37
Q

If a void is accidently discarded during a 24 hour urine collection what needs to happen?

A

RESTART the clock : (

38
Q

What are some of the clinical manifestation of CKD discussed in class?

A

mineral disorder (calcitriol deficiency and hypocalcemia), hyperparathyroidism, hyperphosphatemia, hypertension, proteinuria/diabetic neuropathy, peripheral edema, anemia, metabalic acidosis and hyperkalemia

39
Q

Why does CKD cause hypocalcemia, hyperparathyroidism, and hyperphosphatemia?

A
  1. The kidneys are unable to convert vit D into active calcitriol, thus decreasing the absorption of calcium leading to hypocalcemia.
  2. The parathyroid gland senses low serum calcium levels and secretes more parathyroid hormone, leading to increased bone resorption and bone fractures.
  3. D/t recipricol relationship, decreased calcium leads to decreased excretion of phosphorus.
40
Q

sxs of hypocalcemia

A

tetany, parathesia, chvostek’s sign, Trousseau’s sign, muscle excitability, hyperphosphatemia, dysrhythmias

41
Q

tx for calcitriol and calcium supplements

A

calcitriol and calcium supplements

42
Q

tx for hyperphosphatemia

A
  • phosphate binders: PhosLo and sevelamer

- decrease phosphate food intake: milk, red meats, poultry, fish, beans, nuts

43
Q

how do phophate binders work?

A

They bind to phosphate so that it will be excreted out in feces, decreasing serum phosphate levels.
*PhosLo contains Ca, so can increase Ca levels.

44
Q

How does CKD cause HTN?

A

decreased perfusion of kidneys leads to increased renin release (via RAAS)

  • angiotensin II causes vasoconstriction of arterioles
  • aldosterone release leads to sodium and water retention (increased BV, increased BP)
45
Q

Explain the clinical manifestation of proteinuria and diabetic nephropathy.

A
  • glomerulus become hyperpermeable, allowing protein to pass through and be excreted in urine (proteinuria)
  • loss of protein decreases colloidal osmotic pressure; fluid shifts from the intravascular space: edema, third-spacing
46
Q

Why does CKD cause peripheral edema?

A
  • inadequate filtration excretes protein, decreases colloidal osmotic pressure
  • increased aldosterone causes sodium and water retention leading to hypervolemia
47
Q

The kidneys produce _______, which stimulates bone marrow to produce _______.

A

erythropoietin, RBCs

48
Q

What Hgb and Hct values might you expect with a CKD patient?

A

lower

49
Q

Why does CKD cause anemia of chronic disease?

A

Kidney damage causes a deficiency of erythropoeitin and reducing the amount of RBCs produced by bone marrow.

50
Q

anemia of chronic disease is characterized by RBCs that are: (size and color)

A

normocytic and normochromic

51
Q

tx for anemia of chronic disease

A

erythropoeitin stimulating agents

**require iron stores (or iron supplements)

52
Q

How does CKD cause metabolic acidosis and hyperkalemia?

A
  • impaired ability to excrete acid load
  • defective reabsorption and increased making of HCO3-
  • hyperkalemia: shift of H+ into the cells and K+ out of the cell and impaired excretion of K+
53
Q

The kidneys normally excrete ___-___% of potassium.

A

80-90% - kidney damage leads to decreased ability to excrete K+

54
Q

CKD patients need to monitor K+ intake.

A

True d/t decreased potassium excretion.

55
Q

indication for sodium polysterene sulfonate

A

ongoing maintenance of mild to moderate hyperkalemia

*available in PO and retention enema

56
Q

action of sodium polysteren sulfonate

A
  • exchanges Na+ for K+ ions in the intestine

- eliminated in feces

57
Q

contraindication for sodium polysterene sulfonate

A
  • abnormal bowel function or histor of bowel disorders (e.g. crohn’s, constipation)
58
Q

management of CKD

A
  • managing HTN via antihypertensives
  • diet modification
  • lowering cholesterol
  • optimal glycemic control (prevent DM complications)
  • exercise (3-4/week for 30 min)
  • limiting/avoiding nephrotoxic drugs (e.g. antibiotics)
  • avoiding alcohol
  • smoking cessation
59
Q

dietary modifications to managae CKD

A
  • low sodium: control blood volume
  • potassium monitoring: prevent hyperkalemia
  • protein intake: monitor via labs (albumin, prealbumin, BUN, Cr, total protein)
  • phosphorus restrictions: monitor intake, phosphate binders

Nursing Semester 2 (7 decks)

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