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Spring 2015 > MNT 2 - Exam #3 (Part 1) > Flashcards

MNT 2 - Exam #3 (Part 1) Flashcards

1
Q

What is the prevalence of T1DM?

A
  • 5-10% of all DM cases

- About 5% of these cases are idiopathic

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2
Q

What are the causes of T1DM?

A
  • Immune mediated versus idiopathic;
  • About 5% of these cases are idiopathic
  • Rate of beta cell destruction variable;
  • “honeymoon period”still maintains insulin production;
  • Causes → NOT clearly understood;
  • Multiple genetic predispositions;
  • Environmental factors (coxsackie virus, cow’s milk protein, rubella = possible triggers)
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3
Q

What is the pathophysiology of T1DM?

A
  • Absolute deficiency of insulin = beta cells are totally destroyed and they make none;
  • Elevated plasma glucose
  • Cells cannot use glucose for energy
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4
Q

What are the clinical manifestations of T1DM?

A

S/S”s of body’s efforts to compensate:

  1. Glycosuria – glucose in the urine
  2. Polyuria – excessive urination
  3. Polydipsia – increased thirst
  4. Polyphagia – increased hunger
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5
Q

How is an Oral Glucose Tolerance Test (OGTT) used with T1DM diagnosis?

A

-Oral glucose tolerance test (OGTT)- to dx IGT, IFG, GDM

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6
Q

What are the diabetes related Autoantibodies?

A
  • Glutamic acid decarboxylase autoantibodies (GADA);
  • Islet cell autoantibodies (ICA);
  • Insulin autoantibodies (IAA);
  • C-peptide
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7
Q

What are Glutamic Acid Decarboxylase Autoantibodies (GADA)?

A
  1. Test measures specific islet cell antigens

2. Most sensitive marker for T1DM risk

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8
Q

What are Islet Cell Autoantibodies (ICA)?

A
  • Also indicator or T1DM risk;
  • Will not be as accurate an indicator as the T1 progresses as the antibodies are lost ;
  • Prevalence of ICA decreases as T1DM continues
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9
Q

What are the Insulin Autoantibodies (IAA)?

A
  • Evidence of ongoing Beta-cell destruction

- Not accurate if patient injecting insulin

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10
Q

What are the C-peptides?

A
  • Released as insulin’s 2 polypeptide chains separate

- So c-peptide can be used to measure insulin production

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11
Q

What are the goals of MNT for T1DM?

A
  1. Achieve and maintain optimal BG, BP, and lipid levels
  2. Improve overall health (diet and exercise)
  3. Address individual energy and nutrients needs while considering personal/cultural preferences, lifestyle, and pt’s readiness to change
  4. Prevent or delay, and treat long-term complications of DM
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12
Q

What is the focus of education with T1 Diabetics?

A
  • T1 starts earlier in life so there is a longer lifespan for risk of complications
  • Acute complications and sick day management education is key
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13
Q

What the main MNT approaches for T1DM?

A
  • Integrate insulin therapy with an individual’s food and physical activity
  • Base food plan on assessment of appetite, preferred foods, usual eating and exercise
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14
Q

What are the methods of insulin therapy?

A
  1. Flexible or intensive insulin therapy: (CSII or MDII) → Continuous Subcutaneous Insulin Injections; Multiple daily insulin injections
    — Determine and adjust pre-meal insulin doses based on the total amount of CHO in the meal
    — Test BG 30 minutes prior to a meal and adjust insulin accordingly
    — Use a carbohydrate-to-insulin ratio
  2. Fixed daily insulin dose
    — Emphasize consistency in day-to-day meal CHO content
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15
Q

What are the macronutrient needs with T1DM?

A

-PRO — RDA: .8-1.0 g/kg;

  • Kcals =
    1. Sedentary: 25 kcal/kg
    2. Normal: 30 kcal/kg
    3. Undernourished or active: 45-50 kcal/kg

-Determine fat and CHO intake based on lipids and weight levels

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16
Q

What are the assessment consideration for T1DM?

A
  • Relevant medical history
  • Present health status
  • Diabetes knowledge and skills
  • Cultural influences
  • Health beliefs/attitudes
  • Support systems
  • Readiness to change
  • Barriers to learning
  • Socioeconomic factors
  • Client goals
  • Level of glycemic control
  • Insulin regimen
  • Usual schedule
  • Usual food intake = Meal times, composition, and macronutrient content)
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17
Q

What are the T1DM insulin medical treatments?

A
  1. Syringes or pens
    - Syringes disposable
    - Pens refillable 150-300 U insulin
  2. Insulin pumps
    - Battery powered size of pager
    - Duplicates endogenous insulin best
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18
Q

What are the T1DM goals fro preprandial glucose?

A 
Normal = <100mg/dL
GOAL = 70-130 mg/dL;
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19
Q

What are the T1DM goals fro postprandial glucose?

A 
Normal = < 140mg/dL;
GOAL = <180mg/dL
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20
Q

What are the T1Dm goals for AIC?

A

Normal = 4-6;

GOAL = <7

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21
Q

What is the care plan documentation for T1DM?

A
  • Physician referral for MNT
  • Patient name (ID information)
  • Date of visit/ time spent
  • Reason for visit
  • Current & past Dx
  • Pertinent test/lab results
  • Current medications
  • Others present during visit
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22
Q

Nutrition Assessment for T1DM

A
  • nutrition hx, medical hx, social hx
  • assessed needs for macronutrients/ micronutrients
  • labs/biochemical;
  • nutrition focused physical;
  • for follow up: achievement of goals (behavioral and clinical);
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23
Q

Nutrition Diagnosis and Intervention for T1DM

A

-Nutrition Diagnosis (PES)
-Nutrition Interventions
— Nutrition RX always first
— Food and meal planning
— Short and long term goals (clinical/ behavioral)
— Educational topics covered/ materials provided

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24
Q

Monitoring and Evaluation for T1DM

A
  • Impression of patient acceptance and understanding
  • Anticipated compliance
  • Additional skills or information needed
  • Recommendations and plans for ongoing care
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25
Q

Evaluation for T1DM

A
  1. Weight/Height (q visit)
  2. HgbA1c (Initially, 4-6 wks after changes, then 3-4 times a year)
  3. Lipid profile (initially, 6 months after lifestyle changes, then annually)
  4. Blood pressure (follow up visit)
  5. Self Monitoring (follow up visit) = Food record, BG and medication records (changes in meds?), Activity/exercise patterns
  6. Specific behavior changes per plan (q visit) Schedule changes (follow up visit)
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26
Q

What are the goals for Gestational DM?

A
  • PRE-prandial </= 120
  • When insulin is used, post prandial SMBG is preferred as these values directly R/T rates of macrosomia, neonatal hypoglycemia and C-section.
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27
Q

What is Diabetic Ketoacidosis (DKA)?

A
  • Inadequate insulin = gluconeogenesis
  • Lipolysis stimulated by counter regulatory hormonesà ketones
  • Metabolic acidosis
  • Osmotic diuresis occurs = Dehydration and electrolyte imbalances
  • Hyperglycemia
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28
Q

DKA affects….

A

–

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29
Q

Labs for DKA…

A

–

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30
Q

Treatment and Prevention for DKA…

A

–

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31
Q

What are the 3 steps in CHO counting for pumps?

A
  1. Identify the anticipated CHO intake at meals and snacks
  2. Accurately determine the CHO intake based on grams of CHO or CHO choices or a combination of grams and choices
  3. Administer a rapid-acting or short-acting pre-meal insulin dose based on a pre-determined carbohydrate-to-insulin ratio
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32
Q

What are the insulin requirements for T1DM?

A
  • Type 1DM: (normal weight) 0.5-1.0 units insulin /kg body weight /day
  • 40-50% of total insulin for basal
  • Remainder (rapid acting insulin)- divided for meals
  • Can be divided proportionately to CHO content
  • Or divided as 1-1.5 units of insulin/ 10-15g CHO consumed
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33
Q

What are the insulin requirements for T2DM?

A
  • Type 2 DM: 0.5-1.2 units insulin /kg body weight/ day

- Larger dose may be needed (> 1.5units/kg BW) initially due to insulin resistance;

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34
Q

What can alter dosing of insulin?

A
  • Larger amount often needed to cover breakfast due to effect of morning counter regulatory hormones;
  • Smaller dose may be used when insulin combined with oral meds.
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35
Q

How do you determine total daily insulin requirements?

A
  • Total daily insulin requirement:[ wt (lbs.) divided by 4] or [0.55 X wt (kg)]= units insulin;
  • Dosage divided: 50% basal; 50% rapid with meals;
  • T1DM w/ trace to sm. Amt. ketones or T2DM w/ BMI</= 27: 0.2-0.5 units/kg
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36
Q

How much of daily insulin is BASAL?

A

*Basal: 50% of Total Daily Insulin
-Example: If TDI = 50 units
— 50% of 50 units = 25 units of long acting (or rapid if pump)
— 50% of 50 units = 25 units for bolus (then divided into 3 meals à 8 units/meal)

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37
Q

How much of daily insulin is BOLUS?

A

(Bolus insulin dose may be adjusted for individual meals based on glucose response)

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38
Q

What are CHO to Insulin ratios

A
  • Based on matching the CHO content of food to be eaten with rapid-acting or short-acting insulin
  • Each person can have different ratios
  • CHO: insulin can vary from meal to meal
  • C:I allows pt to figure out how many units of insulin would be needed to cover a meal
  • Could also be used to decrease insulin if decreasing CHO intake in that meal or snack
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39
Q

What are the general guidelines for insulin adjustments?

A
  1. Limit changes in insulin up or down to 1 or 2 units of one insulin (basal or bolus)
    — No more than once in 3-4 days
  2. Adjust only the insulin that affects the abnormal bg value
    — ↑ insulin if bg is too high
    — ↓ insulin if bg is too low
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40
Q

What is Gestational DM?

A
  • Pathophysiology - similar to type 2 DM
  • Decreased islet cell function (decreased insulin secretory response)
  • Peripheral insulin resistance (decreased insulin sensitivity)
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41
Q

What causes GDM?

A
  • Hyperglycemia of GDM due to inability to compensate (with insulin) for:
    1. Increased nutrient needs of gestation
    2. Increased adiposity of pregnancy
    3. Increased secretion of other hormones
  • *Increased maternal blood glucose causes increased fetal insulin production
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42
Q

What hormones can lead to GDM?

A
  • Human placental lactogen
  • Prolactin
  • Cortisol
  • Progesterone
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43
Q

What are the clinical manifestations of GDM for the MOTHER?

A

Increased risk for:

  • HTN (preeclampsia)
  • Polyhydramnios
  • Difficult birth
  • Pre term delivery < 38 weeks
  • Increased rate of C-sections
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44
Q

What are the potential fetal/neonatal complications of GDM?

A
  • Macrosomia (infant birth weight >90th%ile)
  • Hypoglycemia at birth
  • Respiratory distress syndrome
  • Hypocalcemia
  • Hyperbilirubinemia
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45
Q

What is the protocol for testing for GDM?

A
  • Usual testing at 24-28 weeks gestation unless low risk

- High risk → Most people are tested these days

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46
Q

What individuals are considered LOW risk for GDM?

A
  • < 25 years old
  • Normal BW
  • No family hx of Diabetes
  • No hx of abnormal glucose tolerance
  • Not of ethnic race with prevalence of DM
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47
Q

How is GDM tested?

A
  • 50gm oral glucose challenge

- Results of > 135-140mg/dl @ 1 hr. = testing with 100gm. oral glucose load

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48
Q

What is the diagnostic criteria for GDM?

A
  • Diagnosis of GDM: 2 plasma glucose values exceeding:
  • 95mg/dl (fasting)
  • 180mg/dl (1 hr.)
  • 155mg/dl (2 hr.)
  • 140 mg/dl (3hr.)
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49
Q

What are the treatment goals for GDM?

A
  • Achieve and maintain normoglycemia
  • Optimal nutrition for mother and fetus
  • Adequate energy to promote appropriate weight gain
  • Absence of ketosis
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50
Q

How are maternal energy needs assessed with GDM?

A

INDIRECT evaluation with:

  1. Appetite/ intake
  2. Physical activity
  3. Blood glucose/ ketones
  4. Changes in weight
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51
Q

What are the guidelines for weight gain with GDM?

A

SAME as normal pregnancy:

  • Normal BW: 25 – 35#
  • Underweight: 28 – 40#
  • Overweight: 15 – 25#

-Rate of weight gain = 0-2# during first trimester → Little fetal growth and maternal GI discomfort
— or approx. 2/3 # per week

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52
Q

What are the recommendations for weight loss during pregnancy?

A 
NOT generally recommended (risk of ketosis)
- Obese patient with GDM:		
— May decrease kcal. By 30%
— To decrease rate of weight gain
— Monitor for ketonemia
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53
Q

What are the benefits of exercise and GDM?

A
  • Can decrease peripheral insulin resistance

- Can help control fasting and post-prandial glucose

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54
Q

What are the guidelines for CHO with GDM?

A
  • Controlled CHO, but minimum of 175gm/day
  • Limit CHO at breakfast (10-30gm): increased levels of cortisol/ growth hormone early am
  • Lunch and dinner (3-4 CHO servings)
  • Snacks (1-2 CHO servings)
  • Include HS and possibly 2am snack (prevent ketosis)
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55
Q

What are the guidelines for PRO with GDM?

A
  • 0.8gm/kg DBW + 25gm/day

- May include 2-3oz. Protein mid am to decrease hunger / promote compliance

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56
Q

What are the guidelines for fat with GDM?

A

Fat: per energy needs and CV risk

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57
Q

What are the guidelines for multivitamins with GDM?

A

MVI: suggest taking @ bedtime if patient c/o nausea

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58
Q

What is the meal plan for GDM?

A
  • 3 meals and 2-4 snacks
  • Consistent CHO per previous guidelines:
  • CHO counting with exchanges

-Adjust per:
o SMBG,
oChanges in appetite
oChanges in intake

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59
Q

What medications are prescribed with GDM?

A
  • Insulin (with insulin Rx, SMBG recommended post prandially to decrease risk for macrosomia)
  • Some clinics considering metformin
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60
Q

What should be monitored with GDM?

A
  • Weight
  • Appetite/ Intake
  • Fasting ketones
  • SMBG
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61
Q

What are the Blood Glucose Goals with GDM?

A

-pre prandial: </= 120

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62
Q

What are the guidelines for starting insulin with GDM?

A
  • FPG > 105
  • 1hr PPG> 155
  • 2hr PPG> 130
  • To reduce fetal mortality
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63
Q

What is Pregnancy Induced HTN (PIH)?

A
  • Gestational HTN vs Preeclampsia
  • Gestational HTN = BP> 140/90 and no proteinuria
  • Preeclampsia= BP > 140/90 with urinary protein of 300mg/ 24 hrs.
  • Severe preeclampsia= BP >160/110 with 5gm protein/ 24 hrs.
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64
Q

What is Preeclampsia?

A

UNKNOWN etiology;

  • Associated with decreased uterine blood flow secondary to vasospasm
  • Causes decrease in size of placenta/ impaired fetal nourishment
  • Can cause impaired blood flow through the umbilical cord to fetus
  • Can cause damage to maternal organs (liver, kidney, retina, cerebrovascular system)
65
Q

What are the treatments for Preeclampsia?

A
  • NOT a decreased sodium diet
  • NOT use of diuretics
  • These do NOT decrease BP or Proteinuria
  • Possible treatment with Mg supplementation
66
Q

What are the kidney nephrons?

A
  • Functional unit of kidney approx. 1.2 million nephrons in each kidney;
  • contains glomerulus;
  • glomerulus connected to tubules;
  • Each nephron functions separately BUT Coordination of control = If one segment of a nephron is destroyed, the nephron no longer functions
67
Q

What is the primary function of the kidneys?

A

Maintain balance of fluids, electrolytes, and organic solutes through continuous filtration of blood

68
Q

What are the tubules of the kidney?

A
  • Proximal convoluted tubule
  • Loop of Henle
  • Distal convoluted tubule
  • Colleting duct
69
Q

What final concentrations are regulated by the kidney nephrons?

A
  • Electrolytes, osmolality, pH, volume
  • Different segments of tubules differ by type of epithelial cells/permeability
  • Hormonal response
70
Q

Where is Urine Formed?

A
  • Glomerulus = 1st step - where Ultrafiltrate formed
  • Filters approximately 1600 L of blood
  • Approx. 150-200L ultrafiltrate/day
  • Approx. 1.5 L of urine excretion/day
  • Process is mainly PASSIVE (perfusion pressure from heart)
71
Q

What occurs in the Renal Tubules?

A
  • Where most re-absorption occurs
  • Re-absorption: amino acids, glucose, select minerals, water
  • Secretion: of solutes, water
  • Much of this process: ACTIVE (involves ATP)
72
Q

How much urine is excreted daily?

A
  • Fixed solute load of about 600mOsm — Majority = NITROGENOUS waste;
  • Can excrete very concentrated OR very dilute urine
  • Given the fixed solute load & minimum of 500ml concentrated urine — 12L of dilute urine = MINIMUM requirement to function
73
Q

What regulates urine excretion?

A
  • Regulated by vasopressin and RAAS contributes:
    1. Decreased blood volume — secretion of renin = Angiotensinogen 2
    2. Vasocontriction and aldosterone secretion (effects Na+ and K+)
74
Q

What is Oliguria?

A

Urine volume < 500ml/day

75
Q

What is Azotemia?

A
  • Excessive build up of nitrogenous waste (urea, uric acid, creatinine, ammonia);
  • abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient filtering of blood by the kidneys
76
Q

What is Renal Failure?

A

inability of kidney to eliminate daily waste

77
Q

What are the other physiological functions of the kidneys?

A
  1. Maintenance of pH
  2. Production of erythropoietin (EPO)
  3. Maintenance of calcium-phosphorous homeostasis
78
Q

What maintains calcium-phosphorous homeostasis?

A
  • Involves complex interactions of PTH, calcitonin, active Vit. D
  • Involves gut, kidney, bone
79
Q

How do the kidneys help to maintain calcium-phosphorous homeostasis?

A
  1. Production of active form of Vitamin D
    - Calcium absorption at gut
    - Suppression of PTH production (PTH mobilizes Ca from bone)
  2. Elimination of calcium & phosphorous
    - Decreased ability to excrete phosphorous and build up affects parathyroid hormone, calcium levels, neurological function
80
Q

What are the secondary complications of renal dysfunction?

A

Hyperparathyroidism and Renal osteodystrophy

81
Q

What is Renal Osteodystrophy?

A

– generalized BONE disease related to Chronic Kidney Disease

82
Q

How does decreased kidney function cause hyperparathyroidism and renal osteo?

A
  1. Decreased ability of kidney to convert inactive Vit.D to active form = decreased Ca+ absorption at the gut
  2. Decreased reabsorption of Ca+ and decreased excretion of Phosphorous = too LITTLE calcium & too MUCH phosphorous
  3. Increased serum Phosphorous = Increased PTH release = Parathyroid hyperplasia = secondary hyperparathyroidism = RENAL OSTEODYSTROPHY

**Imbalance in Ca and P = Calcification of Soft tissues (Vessels, sexual functions, gland organs, etc.)

83
Q

What are the labs to evaluate kidney function?

A
  1. Microalbuminuria → 30-300mg/24 hour in urine test;
  2. GFR;
  3. Creatinine Concentration;
  4. Urinalysis;
  5. Radiologic evaluation (IVP, MRI, ultrasound)
  6. Biopsy
  7. Clearance Calculations
84
Q

What is GFR?

A

Glomerular filtration rate – rate at which substances are cleared from plasma
— Normal 135-180 L/day (most reabsorbed)
— Used to evaluate kidney health, severity/progression of disease

85
Q

What are Clearance Calculations?

A

-Previously: used endogenous creatinine clearance
-Current standard: Modification of Diet in Renal Disease (MDRD) calculation (p.524)
= Incorporates age; gender; race; ser creatinine,, albumin, & BUN
-Web based calculators

86
Q

What is Chronic Kidney Disease?

A
  • Syndrome in which progressive loss of kidney function occurs
  • NOT reversible
  • Progression to CKD stage 5 (variable rate) → Decision time
  • Renal replacement therapy or transplant
  • Requires medication and specialized diet
87
Q

What is the prevalence of CKD?

A
  • About 11.5% of U.S. adults have evidence of CKD per NHANES
  • 1 in 9 adults in U.S.
  • 20 million Americans
  • Has lead to inclusion of eGFR (estimated GFR) on routine labs reporting serum creatinine
88
Q

What are the causes of CKD?

A
  • *Leading causes: Diabetes, hypertension, or glomerulonephritis
  • Other factors:
    1. Ethnicity: African Americans, Native Americans, Hispanic Americans
    2. Family history
    3. Hereditary factors (PCKD)
    4. Direct and forceful blow to kidneys
    5. Prolonged consumption of OTC painkillers (combo ASA, acetaminophen, ibuprofen)
89
Q

What is the pathophysiology of CKD?

A

Signs and symptoms (related to kidney’s decreased ability to perform normal functions)
1. Hypertension: GFR<`15à Na retention/edemaà HTN
2. Metabolic acidosis: r/t kidney not able to excrete H+ ions
3 .Hyperkalemia → Need to watch potassium intake
4. Azotemia → Nitrogenous waste
5. Microcytic anemia and iron deficiency

90
Q

What are the clinical treatment guidelines for CKD?

A
  • NKF KDOQI evidenced based clinical guidelines (since 1997)- recognized worldwide
  • KDOQI= kidney disease outcomes quality initiative
91
Q

What are the goals of treatment for CKD?

A
  1. Manage symptoms associated with CKD = edema hypoalbuminemia, hyperlipidemia
    — Statin meds., low sodium diet, diuretics,
  2. Treat underlying disease to delay progression
  3. Maintain nutritional stores
92
Q

What are nutritional basics for CKD?

A
  • *Sufficient protein & energy (and adequate fat, CHO);
  • to maintain POSITIVE Nitrogen-balance
  • Diets high in protein and exaggerate the kidney complications
  • Improve plasma albumin and eliminate edema
  • Without adequate albumin in the blood, fluid move into interstitial spaces
93
Q

CKD is due to….

A

INABILITY of kidney to:

  1. Excrete waste
  2. Maintain fluid & electrolyte balance
  3. Produce hormones
94
Q

What is Uremia?

A

“urea in the blood”; excess of amino acid and protein metabolism end products, such as urea and creatinine, in the blood that would be normally excreted in the urine

95
Q

What are the signs/symptoms of uremia?

A
  1. Malaise, weakness
  2. N/V
  3. Muscle cramps, itching
  4. Metallic taste in mouth
96
Q

What is Uremic Syndrome?

A

defined as the terminal clinical manifestation of kidney failure (also called renal failure)

97
Q

What is ESRD?

A

ESRD (end stage renal disease);
-the LAST stage (stage FIVE) of chronic kidney disease (CKD). When CKD, polycystic kidney disease (PKD) or other kidney diseases develop into ESRD, dialysis or a kidney transplant is necessary to live.

98
Q

What are the labs that define ESRD?

A

Labs: typically, BUN > 100mg/dL and Cr of 10-12mg/dL

99
Q

What is the treatment of ESRD?

A

Medical Treatment Options:
1. Dialysis
2. Transplant with immunosuppressant therapy
3. Medical management (that will progress to death)
4 .Erythropoietin and Active form of Vitamin D
**(Psychologic support)

100
Q

What is Dialysis?

A
  • Removal of excessive and toxic by-products of metabolism from the blood
  • Replaces the filtering function of the kidney
101
Q

What are the types of dialysis?

A
  1. Hemodialysis – Conventional daily or nocturnal (outpatient or home) → COMMOM
    2 .Peritoneal dialysis – Continuous ambulatory peritoneal dialysis (CAPD) or continuous cyclic peritoneal dialysis (CCPD)
102
Q

When and why would analysis be initiated?

A
  • Prevent further medical complications due to ESRD
  • S/S = dialysis: pericarditis, uncontrollable fluid build up, pulmonary edema, repeated hyperkalemia, lethargy, coma
  • With less severe S/S (azotemia, N/V)- consider pt needs
103
Q

What factors are involved in dialysis decision making?

A
  • Willingness to travel
  • Availability of family/friends to assist at home
  • Type of water supply to home
  • Capability of patient/family to perform sterile technique
  • Patient’s physical/ medical hx considerations re: vascular/ peritoneal access
104
Q

What other people are involved in dialysis selection?

A
  • Patient
  • Family
  • Physician
105
Q

What is common with both types of dialysis?

A

Hemodialysis (HD), or Peritoneal dialysis (PD) = blood passes across selective, semi permeable membrane exposed to rinsing fluid (dialysate)
— (HD): membrane is manmade
— (PD): membrane = lining of peritoneal wall

106
Q

How does dialysis work?

A
  • Diffusion, ultrafiltration, osmosis= methods by which waste and excess fluid is removed. NO direct contact between dialysate and blood.
  • Fluid and electrolyte balance maintained: via varying ion & mineral content of dialysate
107
Q

What is Hemodialysis?

A
  • “Artificial kidney” : membrane is manmade dialyzer – “

- Permanent access to bloodstream

108
Q

How does Hemodialysis permanently access the bloodstream?

A
  1. Arteriovenous fistula (AVF) = Preferred access:
    — Created surgically
    — Joins radial artery and cephalic vein
    -Requires 4-6 wks. before it can be used
  2. Arteriovenous graft (AVG) = second option - Teflon
  3. Subclavian = temporary route
    **Purpose of fistula/graft: ability to puncture repeatedly
109
Q

What are the Hemodialysis regimen options?

A
  • 3 days/week for 3-5 hrs/ treatment at a center
  • 5-7 days/week for 2-3hrs/tx (DHHD) = lower mortality rate similar to transplant
  • 3-6 nights/week for 8 hrs while sleeping (NHHD)
  • Pro’s/con’s of each – kidney school modules
110
Q

What is Peritoneal Dialysis (PD)?

A
  • Membrane is lining of patients peritoneal wall
  • Access via catheter surgically implanted into peritoneal cavity
  • Dialysate containing high-dextrose concentration is instilled into peritoneum
  • Solutes (waste) from plasma in capillaries in peritoneal wall pass across peritoneal membrane into dialysate (by diffusion)
  • Water moves by osmosis
  • Once dialysis is complete, dialysate is removed from peritoneum
  • Dwell time and number of exchanges is variable
111
Q

What is the difference in Dwell Time and Exchange Times?

A
  • Dwell time = how long the diffusion remains

- Exchanges = how many time inserted and removed

112
Q

What are the types of PD?

A
  1. CAPD — continuous ambulatory

2. CCP — continuous cycling

113
Q

What is CAPD?

A
  • No machine – uses gravity
  • Manually exchanged
  • 4-5 exchanges /day
114
Q

What is CCPD?

A
  • uses machine-cycler-to fill & empty abdomen
  • Done at night
  • May also include do 1 exchange of CAPD daytime (long dwell)
115
Q

What are the advantages of PD?

A
  • More normal lifestyle
  • Avoidance of large fluctuations in labs
  • May extend renal function
116
Q

What are the complications of PD?

A
  • Peritonitis, weight gain (400-800kcal.day from dextrose)

- (Icodextrin: nonabsorbable sugar for longer dwell times, but costly & potential complications)

117
Q

What is the Renal Transplantation?

A

Match immunological characteristics of donor organ with recipient’s

118
Q

What are Major histocompatibility complex (MHC) antigens?

A

Major role in transplant rejection- MHC on transplanted organ that is different than MHC on recipient tissues initiates immune response

119
Q

What are Immunosuppressive Medications?

A
  • Medication provided to transplant patients that suppress the immune system to help prevent organ rejection;
  • Corticosteroids, cyclosporine, others
  • Numerous side effects = N/V, diarrhea, pancreatitis and more
120
Q

What the concerns and complications of CKD?

A
  • Malnutrition
  • CVD
  • Bone disease
  • Anemia
  • Comorbid conditions requiring MNT = HTN and DM
121
Q

What are the goals of of MNT for CKD?

A
  • Prevent & manage symptoms/ complications (manage altered electrolytes, minimize nitrogenous waste)
  • Slow progression
  • Maintain optimal nutrition (prevent protein-calorie malnutrition)
  • **MNT services reimbursable benefit with Medicare part B
122
Q

What is the focus of the nutrition assessment for CKD?

A
  • MALNUTRITION & PEM (protein energy malnutrition)
  • Increases morbidity/ mortality when prior to dialysis
  • Dietary restrictions contribute
123
Q

What is included in the nutrition assessment for CKD?

A
  • PMHx – patient medical history
  • R/O – rule out
  • S/P – status, post-surgery
  • Anthropometrics
  • Nutritional interview (recent changes- appetite/ intake/ elimination)
  • Changes in appetite
  • Reports of S/S related to kidney problems
  • Barriers
  • Physical assess: S/S of deficiency., height and weight
  • Subjective Global Assessment – overall risk for malnutrition
124
Q

What labs are used in assessment for CKD?

A
  • Vitamin D levels and Calcium
  • Iron
  • Magnesium
  • Potassium → Watch for hyperkalemia at later stages; Always a concern with HTN medications
  • Microalbuminuria & Macroalbuminuria
  • Urine Osmolality
125
Q

What are the main nutrients of concern with CKD?

A
  • Protein
  • Energy
  • Calcium, Vit, D, Potassium, Sodium, Iron, etc.
126
Q

What are the common nutrition diagnoses for CKD (IDNT)?

A
  • Inadequate mineral intake
  • Excessive mineral intake
  • Excessive protein intake
  • Inadequate protein-energy intake
  • Imbalance of nutrients
  • Excessive fluid intake
  • Impaired nutrient utilization
  • Altered nutrition-related laboratory values
  • Food-medication interaction
  • Food and nutrition-related knowledge deficit
127
Q

What is focus of nutrition intervention for Stage 1-2 CKD?

A
  1. Focus on co-morbid conditions — diabetes, HTN = Use ACE Inhibitors or ARBs and Initiation of statin treatment is NO longer recommended for patients on dialysis → Only use pre-dialysis
  2. Hyperlipidemia = DO NOT focus on LDL cholesterol as a guide for CKD
  3. Slow progression of CVS
    * *Reassess nutrition status every 1-3 months
128
Q

What is the MNT for Stages 3-4 CKD?

A
  • *AND’s EBNPG (evidence-based) for CKD 2010
    1. Adequate kcal to prevent malnutrition
    2. Adequate protein to maintain muscle mass and serum proteins yet slow progression of CKD
    3. TLC as indicated to manage blood lipids
129
Q

What are the kcal recommendations for Stages 3-4 CKD?

A

→ Very hard with all the restriction to meet needs;

  • Adults not on dialysis: 23kcal./kg - 35 kcal./kg
  • Overweight adults with Diabetes, not on dialysis:1780-1823 kcal.
130
Q

What are the protein recommendations for Stages 3-4 CKD?

A

-For patients with CKD and no DM: 0.6-0.8gm/kg (with GFR<50)
-For patients with Diabetic Nephropathy – 0.8-0.9gm/kg
— Intakes at 0..7g/kg and less may contribute to hypoalbuminemia
-Evidence that 0.7gm/kg slows decline of GFR (for patients without DM Nephropathy)
**No recommendation to restrict protein at stage 1-2

131
Q

What are the additional recommendations for Stages 3-4 CKD?

A

PROTEIN =

  • If adequate energy intake not possible with 0.6g/kg protein restriction, increase to 0.75g/kg
  • Important to weigh benefits of protein restriction with risks of malnutritionà need for close monitoring
  • HTN must be well controlled for patient to receive benefits of protein “restriction”
  • Per DCCT, BG management more important in delaying onset of renal failure than protein restriction (in patients with DM)
132
Q

What are the mineral recommendations or Stages 3-4 CKD?

A
  1. Sodium: < 2.4g/day
  2. Potassium< 2.4g/day
    3 .Phosphorous: 800-1000mg/day or 10-12mg Phos/g Protein when serum Phos >4.6mg/dL
    4 .Calcium: total elemental calcium intake from all sources (diet, supp., binders) – not to exceed 2g/day (generally restriction w/dialysis)
  3. Fluid: based on management of HTN, fluid build up, urine output
  4. Vitamin D: supplement if 1,25 DihydroxyD3 < 30ng/ml
  5. Iron: supplement w/ oral or IV Fe if ser ferritin < 100ng/ml and transferrin saturation < 20%
133
Q

How do you assess malnutrition with Stage 3-4?

A

K/DOQI clinical practice guidelines (stage 4) → Assessing Malnutrition =
— Q 1-3 mo.: ser alb or %Std BW or Subjective Global Assessment
— Q 3-4 mo.: diet interview/food records

134
Q

What are the AND Practice Guidelines for CKD?

A
  • Outcome assessment factors (biochem.,hemat.,anthro.,S/S)
  • Clinical and behavioral outcome goals (r/t assessment factors and behav. goals- be specific)

Ex.of clinical S/S goals: adeq. muscle, minimal GI symptoms, BP within normal limits
Ex. of behav. Goal: energy intake >80% recommended level
Ex. of biochem/hemat.goal: achieves optimal lab values

135
Q

What are the nutrition interventions for Stage 5 CKD?

A

Hemodialysis – high in protein, control intake of potassium, phosphorus, fluids and sodium; Modifications in fat, cholesterol, TG if warranted

Peritoneal Dialysis – more liberalized; higher in pro., sodium, potassium and fluid, limit phosphorus

136
Q

What are the protein recommendations for Stage 5 CKD?

A
  • Protein = 1.2 g/kg (HD) at least 50% HBV
    — Note > ½ pts. On HD w/protein intake < 1.0g/kg
  • PD same except during peritonitis – increase protein
  • Losses increase 50-100% and may remain elevated
137
Q

How is albumin used to assess protein status with Stage 5 CKD?

A
  • Affected by: fluid status, urine pro loss, inflammation/infection
  • Cannot be used alone to assess pro status w/ dialysis
  • *Not the best indicator
138
Q

What are the energy recommendations with stage 5 CKD?

A
  • To prevent catabolism; needs slightly higher; individualized
  • PD- account for kcal in dialysate
  • 24-27 kcal/kg/day average intake vs rec. 30-35kcal./kg
  • *Use 30-35kcals!
139
Q

What are the FAT recommendations with stage 5 CKD?

A
  • Increased risk for CAD and stroke for HD & PD
  • HD typically have normal LDL, HDL, TG
  • PD higher TC, LDL, TG
  • Recommend TLC diet guidelines for both
140
Q

What are the POTASSIUM recommendations with stage 5 CKD?

A
  • 2-3 g/day for HD
  • More stringent if oliguric or anuric
  • Target range 3.5-6.0 mEq/L
  • Counsel on limiting high potassium foods (HD)
  • PD- adjust per serum levels. Generally less need for restriction. May need supplement
141
Q

What are the Fluid and Sodium recommendations with stage 5 CKD?

A
  • *Highly individualized based on residual urine output and dialysis modality
  • Interdialytic weight gain (HD) should not exceed 5% of body weight
  • 2 gram sodium diet
  • Not more than 1 L fluid daily
  • If urine output > 1 L/day, sodium and fluid can be liberalized to 2-4 g and 2 L
  • Also consider BP, Edema, CHF
142
Q

What are the Fluid and Sodium recommendations with stage 5 CKD on PD?

A
  • PD –can remove 2 -2.5 kg fluid/day
  • Fluid allowance: 2 L
  • Sodium 2-4 g
143
Q

What can fluid overload lead to?

A
  1. edema
  2. shortness of breath
  3. HTN
    4 .CHF
    **To limit fluid intake, limit Na intake;
    **Anything that is liquid at room temp is a fluid
144
Q

What are the Phosphorous recommendations with stage 5 CKD?

A
  1. Early CKD: adaptationà increased excretion Phos/ decreased reabsorption
  2. Hyperphosphatemia w/GFR 20-30 mL/min (HD & PD)
    3 .Dietary phosphorus restiction 800-1000 mg/day, < 17 mg/kg IBW
    4 .Phosphate binders; calcium salts
    5 .Limit high calcium foods (to limit phos)
145
Q

What are the CALCIUM recommendations with stage 5 CKD?

A
  • *Why is serum Calcium often low?
  • foods high in Calcium restricted (source of P)
  • Calcium based phos binders can be Ca source
  • Take supplements on empty stomach
  • Limit to 2000 mg/day from all sources
146
Q

What minerals intakes are correlated to commodities with CKD?

A
  • Research support for correlation between elevated serum phosphorus, Calcium X Potassium product, PTH & cardiac deaths in HD pts-
  • Targets for ser Ca, P, Ca X phos product
147
Q

What are the Vitamin and Supplementation recommendations with stage 5 CKD?

A

-Water soluble vitamins =

  • “Renal” vitamins include B12, folic acid, Vit. C
  • Avoid high doses of Vit. A & C (no > 100mg C/d)
  • Excess C can = oxalosis
  • Serum Vit. A already increased w/dialysis (decreased catab., failure of dialysis to remove, increased ser retinol binding protein)
  • May need Vit. K if on antibiotics vs anticoagulant Rx with dialysis
148
Q

What are the Mineral Supplementation recommendations with stage 5 CKD?

A
  1. Magnesium excreted by normal kidney = poss. Elevated Mg; Avoid mg containing phosphate binders, antacids, and supplements
  2. Iron deficiency anemia:
    — rHuEPO during dialysis
    — Fe supplementation
  3. Zinc @ RDA: 15mg/d
149
Q

What is MNT for CVD with CKD?

A
  • More likely to die from CVD than progress to stage 4 CKD
  • Approx. 50% deaths due to CVD in HD & PD pts.
  • High rates of Heart failure, LVH, atherosclerosis
  • Accelerated atherogenesis with dialysis
150
Q

What are the “non-traditional” risk factors for CVD with dialysis?

A
  • Abnormalities in lipid metabolism
  • Hyperparathyroidism
  • Ca & P imbalances
  • Vascular Calcification
  • Malnutrition
  • Oxidative stress/ inflammation
151
Q

Why is CRP elevated with dialysis?

A
  • Elevated CRP common with dialysis
  • reflects pro-inflammatory cytokines which predict decreased ser alb/ assoc. with malnutrition in dialysis
  • Assoc. with increased CV mortality
152
Q

What is the main fat recommendation for Stage 5 CKD and CVD?

A

omega-3 foods twice/week

153
Q

What is the MNT for Secondary Hyperarathyroidism (SHPT)?

A
  • Can progress to severe, intractable forms of bone disease
  • Prolonged PTH exposure → OSTEITIS FIBROSA
  1. Rapid bone turnover
    2 .Excess collagen/ inadequate mineralization
  2. More prone to fracture
  3. Vascular & soft tissue calcification
154
Q

How is SHPT managed?

A
  • Restrict dietary phosphorus
  • Phosphate binders
  • Vitamin supp. (oral or IV)- dosed to prevent over/under suppression of PTH
  • Close monitoring serum levels….
155
Q

How does Stage 5 CKD lead to anemia?

A

Low Hgb due to:
— Inadequate synthesis
— Blood loss w/ HD

156
Q

What is the treatment for anemia with stage 5 CKD?

A
  • Treatment with rHuEPO and iron;
  • Administration IV or SC- HD vs PD
  • Adequate Fe important
157
Q

What can cause EPO unresponsiveness?

A
  • Fe deficiency
  • Malnutrition
  • Infections
  • Chronic inflammation
  • SHPT
  • Chronic blood loss
  • Folate / B12 deficiency
158
Q

What are the Oral (peritoneal dialysis) for anemia treatment with CKD stage 5?

A 
Examples:
•Ferrous gluconate
•Ferrous sulfate
•Ferrous fumarate
•Polysaccharide-iron complex
•Heme iron polypeptide
159
Q

What must be considered with iron supplementation?

A
  • Directions for administration
  • Effect of Fe stores on absorption
  • Side effects of oral Fe supplements

Spring 2015 (14 decks)

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