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Pharmacotherapy 2/3 > Exam 3 > Flashcards

Exam 3 Flashcards

(59 cards)

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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?

Study These Flashcards
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
replete iron stores dose
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
ESA therapy
Epoetin-alpha: HD: IV three times per week with dialysis | PD or ND: SQ once weekly or every 2 weeks
27
Monitoring for ESA therapy
-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
corrected calcium equation
(4.0 - albumin)(0.8) + serum calcium
29
what is the Ca x PO4 goal?
30
treatment of hyperphosphatemia
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
How to treat low vitamin D in G3-4 CKD
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
how to treat SHPT
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
Treatment of metabolic acidosis
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
causes of metabolic alkalosis
``` chloride responsive: gastric fluid loss diuretics chloride unresponsive: hyperaldosteronism severe hypokalemia iatrogenic alkali administration (acetate in TPN, lactated ringers solution) ```
35
Treatment of metabolic alkalosis
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
causes of respiratory acidosis
increased pCO2 due to decreased ventilation or ventilation-perfusion abnormalities
37
treatment of respiratory acidosis
O2 replacement/intubation | replacing HCO3- will worsen hypoventilation by promoting retention of pCO2
38
respiratory alkalosis causes
``` decreased pCO2 due to increased ventilation hypoxia nervousness or anxiety or pain pg CNS injury fever asthma severe anemia CHF ```
39
what is normal plasma osmolarity
290
40
Hyponatremia
290) or hypotonic (serum osmolality
41
acute hyponatremia
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
Na+ needed =
(Na+ desired - Na+ observed) X 60% actual weight (kg) NS is 154 meq/L saline 3% is 513 meq/L
43
treatment for hyponatremia, hypovolemia
normal saline at 125-200 ml/hr (1-2L total) d/c diuretics treat diarrhea/vomiting
44
treatment for hyponatremia, isovolemia
free water restriction to 1L/day demeclocycline (blocks ADH) vasopressin 2 receptor antagonists furosemide if diuretic is needed
45
treatment for hyponatremia, hypervolemia
free water restriction +/- Na restriction IV meds in hypotonic saline vasopressin 2 receptor antagonists furosemide if diuretic is needed
46
Hypernatremia
> 145 meq/L
47
etiology of hypernatremia, hypovolemia
chronic renal failure drugs (loop diuretics, laxatives, mannitol) glycosuria
48
etiology of hypernatremia, isovolemia
``` skin losses (burn, fever) diabetes insipidus ```
49
Diabetes insipidus
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
etiology of hypervolemia and hypernatremia
iatrogenic admin of Na+ | mineralocorticoid excess or hyperaldosteronism
51
treatment for hypernatremia hypovolemia
``` D5W or half saline water deficit (L) = [(Na+ observed/140) - 1](.6 actual weight kg) ```
52
treatment for isovolemia hypernatremia
``` 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
treatment for hypervolemia, hypernatremia
Na+ and fluid restrict thiazide 25 mg/day if diuretic is needed IV meds in D5W
54
treatment for hypokalemia
``` 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
treatment for hypophosphatemia
``` 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
treatment for hypomagnesemia
``` 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
treatment for hyperkalemia
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
treatment for hyperphosphatemia
oral phosphate binder: aluminum hydroxide 30 mL aid, calcium carbonate 4-6 g/day sucralfate 6-12 g/day
59
treatment for hypermagnesemia
furosemide 40 mg IV and normal saline | dialysis

Pharmacotherapy 2/3 (7 decks)

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