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Pharm 343 > CKD > Flashcards

CKD Flashcards

1
Q

Patients at risk for CKD

A

> 60yo (likely in stage 2 from 1ml/year decrease)
HTN or diabetes
family history
nephrotoxic drugs
AKI history
Lupus

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2
Q

GFR >90

A

stage 1

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3
Q

GFR 60-89

A

Stage 2

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4
Q

GFR 45-59

A

Stage 3a

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5
Q

GFR 30-44

A

Stage 3b

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6
Q

GFR 15-29

A

Stage 4

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7
Q

GFR <15 or dialysis

A

stage 5

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8
Q

ACR <3 mg/mmol

A

A1 Normal ACR levels

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9
Q

ACR 3.0-30 mg/mmol

A

A2 moderate increase

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10
Q

ACR >30 mg/mmol

A

A3 severely increased

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11
Q

Diabetes mellitus pathology

A

Na hyperfiltration from glucose load and increased glycosylation of mesangial cells causes causing hypertrophy of mesangial cells and then filtering basement membrane causing glomerular scarring and death. Loss of albumin then leads to edema.

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12
Q

HTN pathology

A

RAAS system activation causes AG2 secretion which constricts efferent arteriole increasing BP, this increases permeability and albuminuria. Aldosterone also causes constriction and causes retention of H2O and Na+. Maladaptive hypertrophy and tubular damage/oxidative stress causes renal failure

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13
Q

CKD progression factors

A

Hyperglycemia
HTN
smoking
obesity
proteinuria (causes inflamm and fibrogenic pathways leading to damage)

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14
Q

CKD symtoms

A

Pericarditis, edema (Aldosterone H2O retention and albumin loss), pruritus from waste, restless leg syndrome from increased electrolytes, cramps, anemia

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15
Q

Diagnosis

A

eGFR <60 and ACR>3 (retest both and order urinalysis)
If GFR is 30-60 and/or ACR 3-60 then no referral
but if GFR <30 ACR >60 or any hematuria then refer

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16
Q

Lifestyle changes

A

Low phosphate and sodium diet
Limit protein to 0.8g/kg G3-G5
limit alcohol to <2 drinks/day
physical activity
smoking cessation
weight management when required

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17
Q
A
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18
Q

ACE renoprotective

A

Shown to reduce progression of albuminuria in normotensive patients with type 1 and 2 diabetes

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19
Q

ARB renoprotective

A

Shown to prevent decline in renal function

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20
Q

ACEi and ARB monitoring

A

-Titrate dose every 3-4 days, watching for BP and proteinuria target.
-A/E, dry cough (ACE), angioedema, hyperkalemia (aldosterone block)
-Hold during sick days
-Expect 25-30% increase of SrCr and GFR decrease in first 1-2 weeks
-Get baseline SrCr and K+ and test Q1-2W for titration then Q3-6M

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21
Q

Proteinuria

A

ACE and ARBs are first line as they reduce hyper filtration
-non-dihydropyridine Ca+ channel blockers are second line
-Spironolactone may be of help in patinents already on ACE/ARB and SGLT2i with normal K+ and GFR >25
-Finerenone, has some efficacy in diabetic CKD and GFR>25

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22
Q

Non-dihydropyridine Ca+ channel blockers CKD

A

Used as second line treatment of proteinuria (diltiazem, verapamil)

23
Q

spironolactone CKD considerations

A

Can be used for persistent proteinuria in patients on ACE/ARB and SGLT2i with normal K+ and GFR >25
- Monitor for hyperkalemia

24
Q

Finerenone

A

has some effect on proteinuria in diabetic CKD with GFR >25

25
Q

SGLT2i

A

First line for glycemic control, Works to slow progression of DM and non DM patients (dapagliflozin)

26
Q

SGLT2i mechanism

A

prevents SGLT2 from glucose and Na up take, this lowers BP and sympathetic activity. Na+ retention causes macua dense to decrease blood flow and slow hypertrophy

27
Q

SGLT2 initiation

A

Do not start if GFR <30, unless DM on ACE/ARB then >20 is ok
-Once on therapy continuation below 20 is fine
-Do not initiate if starting dialysis

28
Q

SGLT2 monitoring

A

-Monitor for GFR decrease which should stabilize after 4weeks, if >20-25% decline F/U and if >30% D/C
-A/E UTIs, increased urination, diabetic ketoacidosis
Check A1c Q6M, want <6.5 or <8 for DM, Anemia can artificially lower A1C

29
Q

Diabetic ketoacidosis Sx

A

difficulty breathing, thirst, confusion, abdominal pain, nausea/vomiting

30
Q

GLP-1

A

second line for glycemic control, can reduce CV outcomes. For use in DM when SGLT and metformin don’t control A1c

31
Q

Statin medications

A

Given to all patients >50yo or 18-49yo with moderate to high risk of CV

32
Q

SADMANS

A

Sick day protection of kidneys
-Sulfonylureas
-ACEi
-Diuretics
-Metformin
-ARBs
-NSAIDs
-SGLT2i

33
Q

Urgent dialysis signs

A

Acidosis
electrolyte imbalance (K+ especially)
Fluid overload causing pulmonary edema
Uremia, causes itch over body from waste

34
Q

CKD anemia

A

Kidneys not longer produce EPO leading to hypo proliferative normocytic and normochromic anemia. Can also be due to lack of iron from inflammatory conditions
- Stage 4 >50% of people have it

35
Q

Anemia testing intervals

A

Stage 3 - Hgb annually
Stage 4-5 every 6 months
Stage 5 on dialysis every 3 months
Increasing frequency when under therapy

36
Q

anemia symptoms

A

fatigue, lethargy, cold intolerance, angina, dizziness, pallor

37
Q

Anemia cardiac impact

A

ventricular volume overload can lead to dilation and hypertrophy increasing mortality of floppy heart.

38
Q

Types of iron

A

Serum iron (bound to transferrin)
Transferrin (iron transport)
Ferritin (main storage in GI)

39
Q

Iron labs

A

Total iron binding capacity (TIBC)
Transferrin saturation (TSAT)
Hgb
Ferritin

40
Q

TIBC

A

total iron binding capacity, indirect measure of transferrin capacity

41
Q

TSAT

A

transferrin saturation, Serum iron/TIBC*100, lets us know how much iron is ready for use by bone marrow

42
Q

Hepcidin

A

Liver produce hormone, degraded and excreted by kidneys. Stimulated by iron uptake, inflammation or infection. Causes reduced absorption and prevents iron release from macrophages, duodenum and hepatocytes

43
Q

Functional anemia

A

You have adequate stores but low mobilization from increased hepcidin or ESA treatment
Normal or elevated Ferritin with TSAT <20%

44
Q

Absolute anemia

A

You have low iron stores and little delivery to bone marrow, low ferritin with TSAT <20%

45
Q

When to start iron therapy

A

When Hgb is low (<120) females (<130) males and TSAT <30% and ferritin <500 ug/LI

46
Q

Iron therapy goals

A

TSAT 20-40% no more than 40%
Ferritin, >100ug/L or >200 for dialysis, and <500

47
Q

Oral iron

A

150-300 elemental iron in divided doses titrated up
Take with food and Vit C
——–
-nausea and vomiting
-Dyspepsia
-constipation
-Can go away with continued therapy
————-
Monitor ferritin, TSAT, Hgb every 3 months Stage 3-5
Or every month for dialysis

48
Q

Fumarate, sulfate and gluconate iron

A

Cheap but need stomach acid for absorption and therefore prefer empty stomach which increases side effects

49
Q

Polysaccaride iron

A

no stomach acid needed so can be taken with or without food (most preferred form)

50
Q

Heme iron

A

More bioavailable and does not need to be taken with or without food

51
Q

Separate iron dose from

A

-Antacids
-Synthroid
-Bidphosphonates
-levodopa/methyldopa
-quinolone or tetracycline antibiotics

52
Q

ESA treatment initiation

A

For dialysis patients with Hgb 90-100, for non-dialysis patients it is individualized choice
-Target is 100-110 and not to be used past 115
-Iron supplementation is required during use
-Epoetin alfa or darbepoetin
-A/E HTN, clotting (stroke), pure red cell aplasia, ESA resistance

53
Q

ESA monitoring

A

Inadequate dose indicated by <10g/L increase in 4 weeks (increase dose by 25%
Overdose is >10 in 2 weeks or >20 in 4 weeks. Decrease dose by 25 or 50%
can also change frequency instead of dose

Pharm 343 (23 decks)

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