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Clinical Nutrition 3 > Kidney Diseases Key Concepts (Midterm Review) > Flashcards

Kidney Diseases Key Concepts (Midterm Review) Flashcards

1
Q

Give 5 signs of early CKD

A
  • Weight loss
  • Itching
  • Swelling in ankles
  • Loss of appetite
  • Vomiting
  • -> Mostly due to their uremic level state which is increasing
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2
Q

Uremic state symptoms?

A
  • Anorexia
  • N/V
  • CNS abnormalities
  • Loss of concentration
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3
Q

There is no _____ between the absolute serum levels of BUN and Cr in the development of Uremic symptoms

A

No

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4
Q

Glucose normal vs dialysis?

A 
Normal = 4.0-6.6
Dialysis = 18-35
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5
Q

UN normal vs dialysis?

A 
Normal = 2.0-9.3
Dialysis = 18-35
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6
Q

CR normal vs dialysis?

A 
Normal = 52-115 
Dialysis = 600-1800
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7
Q

Ca normal vs dialysis

A

Both = 2.15-6.65

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8
Q

Pi normal vs dialysis?

A 
Normal = 0.58-1.32
Dialysis = 0.58-1.7
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9
Q

Normal K vs Dialysis?

A 
Normal = 3.5-5.1
Dialysis = 3.5-5.5
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10
Q

Albumin normal vs dialysis?

A 
Normal = 32-50
Dialysis = 32-50 with goal of 40
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11
Q

High glucose?

A
  • Diabetes
  • Long-standing urea
  • 1-3 hrs post p.o
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12
Q

Side effects of high glucose?

A

Thirst

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13
Q

High urea?

A

-Too much protein

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14
Q

Low urea?

A

-Inadequate protein and /or energy

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15
Q

Side effects of high urea?

A

-Anorexia, N/V, fatigue, bad taste in mouth, hyperkalemia

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16
Q

Side effects of low urea?

A

LBM breakdown

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17
Q

High creatinine?

A
  • Not enough dialysis

- LBM loss

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18
Q

Side effects of high creatinine?

A
  • Anorexia
  • Nausea
  • fatigue
  • Weight loss
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19
Q

High calcium?

A
  • Supplements
  • Vit D
  • High CaIntake
  • HyperPT
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20
Q

Low calcium

A
  • High PO4 intake

- Not taking PO4 binder with meals

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21
Q

Side effects of high calcium?

A

-Muscle weakness, consitipation, fatigue, N/V, anorexia

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22
Q

Side effects of low calcium?

A

-Twitching, cramping, tingling fingers, hair loss, depression

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23
Q

Low albumin?

A
  • Inadequate protein and/or energy

- Recent infection

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24
Q

Side effects of low albumin?

A

-Increased chance of infection, edema, weakness.

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25
Q

High Phos?

A

-Not taking binder w/ meals, too much protein

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26
Q

Low phos?

A

Too much PO4 binder, poor intake

27
Q

Side effects of high phos?

A

-Itching, joint pain, easily broken bones, increased PYH

28
Q

Side effects of low phos?

A

-Muscle weakness

29
Q

High K+

A

-Too much f/v, additives, protein

30
Q

Low K+

A

-Too little f/v, eating poorly

31
Q

Side effects of high K+

A

-MI, arrhythmias, numbness/tingling in hands, death

32
Q

Side effects of low K+

33
Q

Tx if TGs are elevated?

A
  • Reduce refined CHOs, alcohol
  • Add omega-3
  • Reduce BW, exercise
34
Q

Typical lipid patterns in PD?

A
  • Normal Chol
  • High TG
  • Low HDL
35
Q

Why does the creatinine level increase in proportion of LBM breakdown? Why does this change with ethnicity?

A

As it is a product of LBM breakdown

-In African Americans, they have more LBM and therefore are expected to have higher creatinine levels

36
Q

Why abnormal lipid values in dialysis?

A

-Dextrose absorption from dialysate and protein losses into the PD contribute to impaired TG clearance

37
Q

How can a patient compensate for a “salt outing”?

A

By reducing fluid until next dialysis (less hypovolemia)

38
Q

Why may the nutritional diagnosis be due to inadequate food intake?

A
  • Physiological factors (N/V, dysgeusia)
  • Psychological factors (Emotional distress, anxiety)
  • Social barriers (limited income, inability to prepare foods at home)
39
Q

Why may the aetiology of systemic inflammation be related to?

A
  • Dialysis
  • Fluid status/volume overload
  • GI bacterial overgrowth
  • Failed kidney transplant
40
Q

Endocrine disorders associated with uremia?

A
  • Hyperparathyroidism
  • Hyperglucagonemia (Increase glucagon, more gluconeogenesis and glycogenolysis leading to increased BG and insulin resistance)
  • Resistance to the actions of insulin and IGF-1
41
Q

What does metabolic acidosis result in?

A

Increased protein catabolism

42
Q

When does renal bone disease develop?

A

In the early stages of CKD

43
Q

Why do patients with CKD have decreased Ca absorption (2)?

A
  • Altered metabolism of vitamin D

- Inability to excrete phosphate or hyperphosphatemia

44
Q

What does suboptimal calcium and phosphate regulation result in?

A
  • Decreased calcium, or hypocalcemia

- Hyperparathyroidism and renal osteodystrophy

45
Q

What results in secondary hyperparathyroidism?

A 
Failure of the endocrine function of the kidneys to
produce calcitriol (1,25 - dihydroxy cholecalciferol)
46
Q

How should secondary hyperparathyroidism be treated?

A

Supplement with active form of Vit D: to increase
calcium absorption and raise serum calcium level and
suppress PTH secretion

47
Q

How should hyperphosphatemia be controlled through diet? What are key offending items?

A
  • Restrict to Phos of 12 mg/kg/day ORR 15 mg/gPro/day

- Dairy, meat, fish, poultry, legumes, bits, bran, cola, chocolate, beer**

48
Q

Other ways to control hyperphosphatemia?

A
  • Use phosphate binders (Sevelamer –> Renagel –> Calcium free)
  • Avoid aluminum containing binders
  • Take binders with food
49
Q

High calcium and phosphate solutes result in what?

A

-Metastic calcification in soft tissue areas, and can lead to renal osteodystrophy

50
Q

Aluminum hydroxide as a phos binder?

A
  • Increases plasma aluminum in patients with HD and PD

- Aluminum is toxic at low concentrations - linked to dementia

51
Q

Calcium based salts as a phos binders?

A
  • Not to be used in hypercalcemia

- Contributes to calcium deposit functions

52
Q

Sevelamer (RENAGEL or RENVELA) as a phos binder?

A
  • Safe due to low absorption
  • Lowers LDL
  • Gi disturbances do not use in bowel obstruction
53
Q

Lanthanum (Phosrenol) as a phos binder?

A
  • Lanthanum accumulation can become a problem

- Expensive

54
Q

____ is a clinical consequence of CKD

55
Q

What is anemia caused primarily by?

A

Decreased production of the EPO hormone in the kidney

56
Q

Secondary causes of anemia?

A
  • Residual blood loss in the dialyzer
  • Inflammation due to infection and co-morbid conditions
  • Hyperparathyroidism can be adjunctive cause
57
Q

Treatment with anemia?

A
  • Treat with EPO injections and adequate iron from IV dextran
  • Return blood to patient as much as possible
  • Treat hyperparathyroidism
  • Avoid blood transfusions which may help prevent iron overload and antibody production which may prevent successful transplantation later
58
Q

Why is constipation common in dialysis?

A
  • Low fluid intake
  • Inactivity
  • Use of calcium containing phos binders
  • F/V avoidance due to k content
  • Low fibre food choices
59
Q

What can severe constipation lead to?

A

Impaction and bowel perforation

60
Q

How should we treat constipation?

A
  • Add foods high in fiber content
  • Increase fluid intake if possible
  • Add fibre in form of psyllium hydrophillic mucilloid (Metamucil)
  • Use stool softener (Docusate Sodium/Colace)
61
Q

During dialysis, how is BP affected?

A

Causes hypotension

62
Q

What does food ingestion during dialysis cause?

A

-Decreased constriction of resistance vessels in certain vascular beds, especially splanic beds - which can last for 2 hours

63
Q

Guidelines regarding food ingestion and dialysis?

A

-Avoid food just before and during dialysis if prone to hypotension

64
Q

Diabetics not prone to hypotension may eat what during dialysis?

A
  • Low fat meal, or use small CHO snack food; fruit, crackers

- Avoid a hypoglycemic episode

Clinical Nutrition 3 (30 decks)

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