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Pharmacotherapy 2/3 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

AKI risk factors:

Patient Susceptibility

A 
per KDIGO:
dehydration
> 60 y.o.
female gender
black race
chronic diseases 
-heart or respiratory failure
-diabetes, cancer, anemia
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2
Q

AKI risk factors:

Exposures

A 
per KDIGO:
pharmacologic agents: (contrast media, nephrotoxic drugs [chemotherapy, saids, ACE-I, ARBs, antimicrobials like ahminoglycosides]])
acute infection (sepsis)
Critical illness/shock
Burns, trauma
surgery
rhabdomyolysis
blood vessel thrombosis
intoxications
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3
Q

AKI definition

A

per KDIGO
increase in SCr by 0.3 mg/dL w/in 48 hours OR
increase in SCr to 1.5 times baseline w/in 7 days OR
urine volume 0.5 mL/kg/h for 6 hrs

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4
Q

staging of AKI

A

per KDIGO
Stage 1: SCr 1.5 - 1.9 times baseline or >/= 0.3 mg/dL increase OR urine output of /= 12 hrs
Stage 3: SCr 3 times baseline OR increase in SCr to >/= 4.0 mg/dL OR initiation of renal replacement therapy OR in patients /= 24 hrs OR anuria for >/= 12 hours

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5
Q

Functional/Pre-renal Failure presentation

A

increased SCr

Oliguria (

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6
Q

types of kidney damage causing intrinsic acute renal failure

A 
damage to:
renal vasculature
glomeruli
tubules
interstitium
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7
Q

Intrinsic Renal Failure presentation

A

Oliguric or non-oliguric (urine > 500 mL/day)
dilute appearing urine or discolored urine
casts & cellular debris
urinary RBC or WBC
higher FEna than pre-renal
lower BUN/SCr compared to pre-renal

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8
Q

Drug induced post-renal ARF

A 
acyclovir
topiramate
methotrexate
indinavir
trimethoprim/silfamethoxazole
anticholinergic medications
cocaine

post renal? taca-tim

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9
Q

Post-renal presentation

A 
Increased SCr
Urine output will depend on extent of obstruction
urine crystals
cellular debris
variable FENa and BUN/SCr ratio
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10
Q

Goals of therapy for acute renal failure

A

Minimize insult to kidney
shorten time to renal function recovery
provide supportive measures until kidney function returns
restore renal function to baseline function

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11
Q

General treatment approach for pre-renal, intrinsic and post renal AKI

A 
Pre-renal:
-hemodynamic support
-volume replacement
Intrinsic:
-remove cause & supportive care
-interstitial damage: remove inciting agent, immunosuppressive therapy (e.g. steroids)
Post renal:
-remove obstruction
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12
Q

what is the fluid dose for prerenal

A

250ml - 2L bolus then 75ml-200ml/hour maintenance

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13
Q

Electrolytes we worry about

A

Hypernatremia (no more than 3g/day of sodium)
Hyperkalemia*** (potassium is 90% renally eliminated - can lead to cardiac arrhythmias, reduce potassium intake)
Magnesium
Phosphorus

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14
Q

How to treat Hyperkalemia

A

(normal value is 3.3-5 mEq/L)
if serum potassium > 6mmol/L, life threatening
1. determine urgency by ECG & k level
2. reverse neuromuscular and cardiac effects with calcium gluconate 1 g. IV push
3. Shift K+ into ICF:
-regular insulin 0.2 units/kg IV/SQ and glucose 100mL D50W
-sodium bicarbonate 1 amp (44 men) IV push
-Beta 2 agonists
4. Removal of K+ from body:
-sodium polystyrene sulfonate (Kayexalate)(Na+-K+ exchange resin) 30 g po/pr q6-8 hrs x 3-4 doses
-dialysis

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15
Q

Indications for Acute Renal Replacement Therapy (RRT)

A 
A - Acid-base abnormalities
E - electrolyte imbalance
I - intoxications
O - fluid Overload (pulmonary edema)
U - Uremia
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16
Q

Risk factors for contrast induced nephropathy

A

CKD (pre-existing renal dysfunction)
diabetes
heart failure (EF 60 per AHA; > 75 per CIN risk score)
hypotension
intra-aortic balloon pump
anemia
others: dehydration, concurrent nephrotoxins, metabolic syndrome, hypertriglyceridemia, hypertension, etc.

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17
Q

How to manage Edema in CKD

A
  1. Dietary sodium restriction:
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18
Q

How to manage Hyperkalemia in CKD

A 
Acute therapy depends on K+ level, rapidity of K+ rise, presence of symptoms/ECG changes
Chronic management: 
-dietary K+ restriction for all patients
-treat underlying cause if possible
-use diuretics if appropriate
-use binders chronically
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19
Q

Acute management of hyperkalemia in patients with CKD

A
  1. Dialysis - use when failure to respond to other therapies or patient is already on dialysis
    2. IV calcium gluconate, use when K+ >/= 7.0 mmol/L - stabilizes the myocardial cell membrane does not remove K+ only lasts about an hour
  2. Insulin + glucose” shifts K+ extracellular to intracellular - in combo w/calcium gluconate or alone Use when K+ 7.0 mmol/L
  3. Inhaled beta agonist - shifts, use when K+ >/= 7 mmol/L but no ECG changes, no IV access
  4. Sodium polystyrene sulfonate oral suspension (Kayexalate): cation-exchange resin (removes K+), 15g/60mL 1-4 times daily
  5. Patiromer sorbitex calcium powder for oral suspension: potassium binder (removes K+), FDA indicated for tx of hyperkalemia (not for emergency or life-threatening), 8.4-25.5 g diluted in 90 mL water taken once daily w/food, administer other oral meds 6 hrs before after,
    SE: constipation, diarrhea, hypomagnesemia, nausea
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20
Q

How to manage metabolic acidosis in CKD

A

consider treating if bicarb

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21
Q

What are the primary and contributing causes of anemia?

A

primary: decreased production of EPO in kidneys
contributing causes:
uremic toxins inhibit erythropoiesis
reduced red cell life span
iron deficiency
other nutritional deficiencies (folic acid & vitamin B12)
Blood loss (GI tract)

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22
Q

how do you diagnose anemia in CKD?

A

Hgb

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23
Q

what are the goals of therapy for anemia?

A

prevent or reverse signs/symptoms and complications
improve survival
improve QOL
reduce need for red blood cell transfusions

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24
Q

what are the steps of managing anemia?

A

(KDIGO)
1. replete iron stores if low:
- documented anemia with or without ESA if: % SAT = 30% AND ferritin = 500 AND increase in Hgb concentration or decrease in ESA dose is desired (per KDIGO)
-1-3 month trial of po iron for G3-5 CKD
-IV iron for G5 CKD on dialysis
2. consider ESA (erythropoiesis stimulating agent)
for dialysis: consider when Hgb is b/t 9-10 g/dL to keep it from falling below 9 g/dL
Non-dialysis: Hgb

25
Q

replete iron stores dose

A

200 mg/day elemental iron in divided doses (ferrous sulfate 325mg po tid)
IV: Ferumoxytol 510 mg IVP followed by 510 mg IV 3-8 days later - for all kinds of dialysis

26
Q

ESA therapy

A

Epoetin-alpha: HD: IV three times per week with dialysis

PD or ND: SQ once weekly or every 2 weeks

27
Q

Monitoring for ESA therapy

A

-use lowest ESA dose that reduces the need for red blood cell transfusions (no goal Hgb)
HD and PD: reduce or hold therapy if Hgb > 11 g/dL
ND: reduce dose or hold therapy if Hgb > 10 g/dL

28
Q

corrected calcium equation

A

(4.0 - albumin)(0.8) + serum calcium

29
Q

what is the Ca x PO4 goal?

A
30
Q

treatment of hyperphosphatemia

A

dietary restriction (avoid milk, cheese, eggs, beans, chocolate, beer, carbonated beverages, meats, peanut butter, shell fish, yogurt, ice cream)
start early in G3CKD & reduce intake to 60% of normal
when GFR 7 or corrected calcium > 11
600 mg po w/meals +/- snacks

31
Q

How to treat low vitamin D in G3-4 CKD

A

measure 25-OH D levels if PTH is above recommended range
if /= 30 ng/mL, maintenance therapy 1000-2000 D3 daily
watch for hypercalcemia

32
Q

how to treat SHPT

A

activated vitamin D (1,25 dihydroxyvitamin D2 or 3)
for G4-5 CKD with persistently high PTH levels and/or hypocalcemia despite normal 25-OH levels
decreases PTH synthesis by direct effect on gland
increases calcium & phosphorous absorption from the gut
don’t use if calcium or phosphorous are above target ranges
Calcitriol PO daily or TIW
IV TIW w/dialysis

33
Q

Treatment of metabolic acidosis

A

acetate in TPN
for chronic treatment: NaHCO3 tablets or Shohl’s solution - divided doses for total daily dose of 24-48 mEq
acute treatment: add 3 ampules NaHCO3 to 1000 mL D5W

34
Q

causes of metabolic alkalosis

A 
chloride responsive:
gastric fluid loss
diuretics
chloride unresponsive:
hyperaldosteronism
severe hypokalemia
iatrogenic alkali administration (acetate in TPN, lactated ringers solution)
35
Q

Treatment of metabolic alkalosis

A
  1. correct underlying cause, correct hypokalemia (20-60 mEq K+ infused over 3 hours)
  2. volume replacement with NS or chloride replacement
  3. Acetazolamide (carbonic anhydrase inhibitor)
  4. PPI or H2RA
  5. severe cases = IV HCl or arginine HCl
36
Q

causes of respiratory acidosis

A

increased pCO2 due to decreased ventilation or ventilation-perfusion abnormalities

37
Q

treatment of respiratory acidosis

A

O2 replacement/intubation

replacing HCO3- will worsen hypoventilation by promoting retention of pCO2

38
Q

respiratory alkalosis causes

A 
decreased pCO2 due to increased ventilation
hypoxia
nervousness or anxiety or pain
pg
CNS injury
fever
asthma
severe anemia
CHF
39
Q

what is normal plasma osmolarity

A

290

40
Q

Hyponatremia

A

290) or hypotonic (serum osmolality

41
Q

acute hyponatremia

A

0.5 meq/L/Hr unless seizures/coma or extreme breathing difficulties, then 1-2 ml/kg/hr of saline 3% with furosemide if CHF present
too rapid correction causes seizures and pontine myelinolysis

42
Q

Na+ needed =

A

(Na+ desired - Na+ observed) X 60% actual weight (kg)
NS is 154 meq/L
saline 3% is 513 meq/L

43
Q

treatment for hyponatremia, hypovolemia

A

normal saline at 125-200 ml/hr (1-2L total)
d/c diuretics
treat diarrhea/vomiting

44
Q

treatment for hyponatremia, isovolemia

A

free water restriction to 1L/day
demeclocycline (blocks ADH)
vasopressin 2 receptor antagonists
furosemide if diuretic is needed

45
Q

treatment for hyponatremia, hypervolemia

A

free water restriction +/- Na restriction
IV meds in hypotonic saline
vasopressin 2 receptor antagonists
furosemide if diuretic is needed

46
Q

Hypernatremia

A

> 145 meq/L

47
Q

etiology of hypernatremia, hypovolemia

A

chronic renal failure
drugs (loop diuretics, laxatives, mannitol)
glycosuria

48
Q

etiology of hypernatremia, isovolemia

A 
skin losses (burn, fever)
diabetes insipidus
49
Q

Diabetes insipidus

A

central = decrease in ADH
nephrogenic = resistance to ADH
central (drugs like ethanol and phenytoin), nephrogenic (drugs, chronic renal failure, hypokalemia, hypercalcemia, sickle cell anemia, autoimmune diseases)
high sodium, high glucose - looks like diabetes because losing water which makes serum sodium serum glucose go high

50
Q

etiology of hypervolemia and hypernatremia

A

iatrogenic admin of Na+

mineralocorticoid excess or hyperaldosteronism

51
Q

treatment for hypernatremia hypovolemia

A 
D5W or half saline
water deficit (L) = [(Na+ observed/140) - 1](.6 actual weight kg)
52
Q

treatment for isovolemia hypernatremia

A 
Nephrogenic: chorpropamide (sensitizes ADH receptor), 200-500 mg/day
carbamezapine 400-600 mg/day
thiazide 25 mg/day if diuretic is needed
D5W
central: DDAVP/vasopressin
thiazide 25 mg/day
D5W
53
Q

treatment for hypervolemia, hypernatremia

A

Na+ and fluid restrict
thiazide 25 mg/day if diuretic is needed
IV meds in D5W

54
Q

treatment for hypokalemia

A 
IV if K = 2.5 meq/L, arrhythmias, muscle spasms, or no enteral route available
PO: 20-40 mEq/day
IV: KCl vs K2PO4
-40-80 men
-administer at rate
55
Q

treatment for hypophosphatemia

A 
IV if phase = 1.0, arrhythmia, CNS disturbances, respiratory difficulties, or no enteral route available
PO: 15-60 mmol/day
IV: Kphos vs Naphos
- usual 15-60 mmil
- administer at rate
56
Q

treatment for hypomagnesemia

A 
IV if Mg = 1.0, arrhythmias, CNS disturbances or no enteral route available
PO: 8-80 mEq/day
IV: Magsulfate
-2-8 g
administer @ rate
57
Q

treatment for hyperkalemia

A

determine urgency by ecg, K level, chronicity
reversal of neuromuscular and cardiac effects: administer calcium gluconate 1 g IV push
shifting K+ into ICF:
administer regular insulin 0.2 units/kg IV/SQ and glucose as 100mL D50W
sodium bicarb 1 amp IV push
removal of K+ from body:
sodium polystyrene sulfonate 30 g po/q 6-8 hrs X 3-4 doses
dialysis

58
Q

treatment for hyperphosphatemia

A

oral phosphate binder: aluminum hydroxide 30 mL aid, calcium carbonate 4-6 g/day
sucralfate 6-12 g/day

59
Q

treatment for hypermagnesemia

A

furosemide 40 mg IV and normal saline

dialysis

Pharmacotherapy 2/3 (7 decks)

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