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Renal Systems > CKD wk 2 & half of wk 3 > Flashcards

CKD wk 2 & half of wk 3 Flashcards

1
Q

How common is CKD?

A

Very common and rising. More common than liver disease; but not focused on that much.

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2
Q

What is the best available screening test for CKD? Why is this superior to eGFR?

A

a. Urine protein or albumin: need to confirm single abnormal test in 1-2 months
b. For both SCr & eGFR: by the time they are abnormal, it’s too late

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3
Q

Why does albuminuria increase the risk for cardiovascular disease?

A

a. Albuminaria correlates w/ angiographic coronary atherosclerosis
b. Baseline albuminuria predicts long term CV morbidity, mortality in patients with HTN

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4
Q

How does proteinuria itself contribute to kidney damage?

A

Proteinuria will disrupt the charge gradient across the glomerular membrane. This is thought to be a main filtration barrier, so disrupting it will cause even more mal-filtration.

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5
Q

What are realistic outcomes of CKD patients by stage?

A

a. Early disease (stage I): stabilization, improvement IF causes are removed
b. Moderate disease (stages II, III): stabilization, mild improvement, difficulty removing causes thus frustration
c. Severe disease (stages IV, V): progressive but delayed decline, improvement in health while on dialysis

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6
Q

What are the risk factors for CKD?

A

a. SAD, obesity, smoking, sedentariness

b. Main etiologies are: diabetes, HTN, glomerulonephritis, idiopathic, cystic kidney disease

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7
Q

What is the overall goal of diet in patients with stage III or less CKD?

A

Whole-food, plant centered diet. Consider low carb/high protein but lower iron diet in patients w/ diabetic nephropathy

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8
Q

When should you intervene to limit potassium in a CKD patient’s diet? What other intervention besides potassium limitation can be used to reduce serum potassium?

A

a. Limit K in late stage disease (IV, V)

b. Other intervention: Glycyrrhiza glabra

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9
Q

When should you intervene to limit phosphorous in a CKD patient’s diet? What other interventions besides a lower phosphorous diet can be used to reduce serum phosphorous and iPTH?

A

a. Also recommended in late stage disease (IV, V)

b. Other ways to decrease phosphate: calcium acetae or carbonate, sevelamer, and lanthanum, niacinamide (B3)

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10
Q

How is calcitriol safely utilized? How are patients taking calcitriol properly monitored?

A

a. Calcitriol is indicated when 1,25D3 is low & iPTH is high
b. Target spot urine Ca2+ is <350 mg

  • Intact parathyroid hormone levels higher than 50 pg/mL in patients with stage 3 or 4 CKD are associated with an increased risk of death or need for renal replacement therapy.
  • *iPTH is Secreted when the calcium level is low.

Give Calcitriol–>b/c–>Dec. Ca2+=>Dec. Vit. D=>Inc. iPTH=> >50 = Death & renal replacement therapy)

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11
Q

How is the renin-angiotensin-aldosterone axis dysregulated in patients with CKD? What can be done to offset this?

A

In CKD, the renin-angiotensin aldosterone system is causing too much aldosterone to be formed, leading to too much water and sodium retention; this will cause GFR to decrease.

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12
Q

Be familiar with ACE inhibitor and angiotensin receptor blocker (ARB) drugs.

ACE INHIBITOR–> slows (inhibit) the activity of the enzyme ACE, which decreases the production of angiotensin II. As a result, blood vessels enlarge or dilate, and blood pressure is reduced.

A
  • **ACE inhibitors: benazepril, captopril, enalapril, quinapril, Ramipril most studied in CRF.
    1. SE: cough main one, rare ones are hypotension, hyperkalemia, elevated SCr
    2. Natural ACEi: lespedeza capitata (Round-headed Bush Clover), crataeus spp.(Hawthorn), allium sativum, gandoerma lucidum (reishi mushroom), hibiscus sabdarifa (Roselle), quercetin (flavonol)
  • **ARB: losartan, irbesartan, candesartan, valsartan
    1. SE: orthostatic hypotension, HA, hyperkalemia, increased SCr
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13
Q

How do G and A stages differ for characterizing CKD? Who defined these stages?

A

G refers to GFR

A refers to albuminuria

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14
Q

What are the different GFR staging #’s?

A 
G1a, >105 (Norm)--> (Norm GFR: >100 men or >90 women)
G1b, 90-104 (Slightly low)
G2a, 75-89 (Mild)
G2b, 60-74 (Mild)
G3a, 45-59 (Mild-Moderate)
*G3b, 30-44 (Mod-Sev)
*G4, 15-29 (Sev)
*G5, <15 (Kidney failure)
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15
Q

What are the A ( albuminuria) staging #’s?

A 
A1a= <10mg/g
A1b= 10-29
A2= 30-299
A3a= 300-1,999
A3b= >2000
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16
Q

When should dietary protein be restricted in patients with CKD?

A

From Brignall: when patient transitions to Stage 4

17
Q

What are nephroprotective herbs? When are they indicated? How do they work?

A

a. Urtica dioica (seed), rheum palmatum, parietaria officinalis, Silybum marianum (seed), orthosiphon stamines
b. They are indicated in early stage kidney disease
c. Some are kidney trophorestoratives, mild diuretics, increase creatinine

18
Q

What parameters should you monitor in patients with stage III CKD and worse? How often? How about stage I and II CKD?

A

Stage 1 & 2: Bun/creatinine, albumin, GFR

Stage 3: In addition to above; Sodium, potassium, calcium, phosphate; blood pH, carbon diozide

19
Q

Should patients with CKD take vitamin D3? Why or why not?

A

Start to have Ca wasting at Stage 3 and PTH will go up as a response. Once this happens, activated D3 is recommended.

20
Q

Why do patients with late-stage CKD have anemia? How is this remedied? Is this a problem in early-stage CKD?

A

a. Nephron loss causes endocrine dysfunction causing loss of EPO leading to anemia
1. Can be remedied w/ EPO (but high toxicity)
2. Adaptogens & bone marrow herbs: panax, atracytylodes macrophala, wolfipori cocos, Glycyrrhiza, angelica sinensis, astragalus

b. Can be a problem in early stage CKD, but need differentiate what the cause is

21
Q

What is the potential toxicity of erythropoietin and similar agents? What is the target hemoglobin in anemic patients with late-stage CKD?

A

a. EPO potential toxicity is increasing CV events when used

b. Hemoglobin target: 10-12 g/dl

22
Q

What is an appropriate overall protocol for patients with stage I and II CKD? How does etiology change this protocol?

A

Treat the cause and prevention. Treat diabetes, HTN to prevent CKD from progressing. Focus on whole foods, plant based diet, exercise, stress reduction.

23
Q

What is an appropriate overall protocol for patients with stage III CKD? How does etiology change this protocol?

A

Still manage causative factors, calcium wasting, electrolyte balances, kidney tonics, etc.

24
Q

What is an appropriate overall protocol for patients with stage IV and V CKD? How does etiology change this protocol?

A

Limit potassium, sodium, etc. Likely to switch to more carbohydrate based nutrition. Monitor closely for when dialysis will be used.

25
Q

Management issues in earlier stages:

Calcium Homeostasis:

A

Ca wasting begins in stage 3 of kidney failure

  1. PTH levels go up–>inc. phosphorus absorption from food
  2. Treating w/calcium or activated Vit. D can cause hypercalcemia–>HTN–>worsening kidney disease
26
Q

Management issues in earlier stages:

Anemia Management:

A

Ferritin >70 makes IDA (Iron deficiency anemia) unlikely.

<70=>National kidney foundation recommends EPO “erythropoietin”

27
Q

Management issues in earlier stages:

Protein Intake Management:

  • Low protein diets have been traditional in treatment of mild-late stage renal failure
  • No benefit from protein restriction was seen

** As disease progresses, whole food diets can be a concern d/t potassium**

A

Dietary protein elevates GFR, you’ll see quick but small drop in GFR

Biological value protein: Speaks to digestibility of protein + rate limiting essential amino acid in proportion to an index protein source (generally egg albumin)

*Management:
(Choose mineral management over protein management)

*Limit to 0.6 g/kg/day. Sourced from high biological value protein (generally egg albumin)

  1. Animal foods have highest biological value
  2. Dairy & eggs over 90%
  3. Meat & fish tend to be 70-80%
28
Q

Management issues in earlier stages:

Sodium restriction:

A
  1. Benefits of sodium restriction magnified; d/t risk for edema & need for BP medications
  2. Aim for 2 g/day

***Caution: if on restriction & develop hypotension or creatinine goes up, stop restriction

29
Q

Management issues in earlier stages:

Medications worsen kidney disease

A

Fluroquinolone antibiotics, NSAIDs, opiates, chemotherapy, contrast media, ACEi or ARBs, protease inhibitors, diuretics, street drugs

30
Q

Management issues in Advanced Stages:
(progressing 4–>5)

Alkali management: recommended for CO2 <22mM

A

a. TX: sodium citrate or sodium bicarbonate

b. Shown to slow nephropathy & important for bone mineralization

31
Q

Management issues in Advanced Stages:
(progressing 4–>5)

Electrolyte balancing:

A
  1. Potassium abnormalities indicate end stage renal failure
    a. K <6 can be managed w/ low K diet
    b. K >6 urgent and dialysis may be imminent
  2. Phosphorus restrictions below 1g/day
  3. Hyperchloremia may occur secondary to bicarb loss
  4. Hypermagnesium can occur late stage
    a. GFR <15 want to avoid supplements
32
Q

Management issues in Advanced Stages:
(progressing 4–>5)

Dialysis:

A
  1. Assessing need: either stage 5, symptomatic or difficult to control stage 4
  2. Electrolyte imbalances
    a. Sodium & phosphorus restriction are important
  3. Protein calorie malnutrition
    a. 1.2-1.5 g/kg/day (1/2 biological value protein)
  4. Vitamins
    a. B, C, D, Ca likely to be at risk
    b. Phosphorus, K, A likely to be very high
33
Q

Biotin (Vitamin B7)

A
  1. Cofactor for carboxylation enzymes. Needed for histones & DNA replications
  2. Dietary sources: legumes, nuts, root vegetables
  3. Functions: utilization of insulin, elongation of fatty acids
  4. Major uses: blood glucose regulation, pregnancy
  5. Other uses: diabetic neuropathy, hemodialysis support, hypertriglyceridemia, brittle nails, loss of sense, cradle cap
  6. Dosing: 30 mcg/day
34
Q

Folate (Vitamin B9)

A
  1. Dietary sources: legumes, FDA fortification, green vegetables
  2. Functions: proper genetic replication, production of normal blood cells, NOS system, one carbon metabolism, production of neurotransmitters
  3. Major uses: prevent neural tube defects, high homocysteine, cancer prevention, cognitive decline
  4. Other uses: depression, RLS, gingivitis, HTN, fatigue, osteoporosis, schizophrenia, bipolar
  5. Negative results: stroke prevention, end stage renal disease/mortality
  6. Toxicity: 1000 mcg/day
35
Q

Renal Failure Symptom management:

A
  1. Fatigue (exercise, L-carnitine)
  2. HTN (do not use K heavy diets, Na restriction)
  3. Cardio risk (N-acetylcysteine)
  4. Depression (folic acid/B12/B6) (be wary of SJW)
  5. Leg cramps (Vitamin C, E)
  6. Dysgeusia (Zinc)
  7. Herkalemia (glycyrrhetinic acid)
  8. Pruritis (Omega 3, activated charcoal, UV light therapy, topical capsaicin)
  9. Uremic neuropathy (B6, B12, biotin, low AGE diet)

Renal Systems (11 decks)

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