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Clinical Pharmacology I > Exam 3 - Renal and Uro Part 1 > Flashcards

Exam 3 - Renal and Uro Part 1 Flashcards

1
Q

ACUTE KIDNEY INJURY

A

ACUTE KIDNEY INJURY

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2
Q

2 categories/criteria used for assessing AKI:

A
  1. RIFLE category

2. AKIN Criteria

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3
Q

Which type of AKI has the highest incidence, is multifactorial, and accounts for 30-90% of mortality rates?

A

ICU Acquired

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4
Q

What are the 3 types of etiologies of AKI?

A

1) Prerenal: decreased perfusion with undamaged parenchymal tissue
2) Intrinsic: structural damage to kidney
3) Postrenal: obstruction of urine flow downstream of kidney

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5
Q

Prerenal AKI is due to what drugs?

A

ACEI/ARB’s
NSAID’s
Vasopressors

Diuretic/Sepsis

It is REVERSIBLE!

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6
Q

When there is an insult to the kidneys, what happens to GFR and Cr?

A

GFR drops

Cr raises

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7
Q

How can AKI be prevented?

A

Adequate fluid intake (2L/day)
Avoid nephrotoxic medications

HYDRATION!
-Crystalloids > Colloids unless pt is low in serum protein

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8
Q

Which Crystalloid is preferred and why? (AKI)

A

0.9% NaCl = isotonic

D5W is also isotonic but it’s all in free water, vascular to intracellular, NOT used as often

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9
Q

Which type of diuretics were not found to be helpful in the prevention of AKI and are only good for managing fluid overload?

A

Loop diuretics

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10
Q

Vasodilators are used in the prevention of AKI, which one is used the most?

A

Dopamine

  • Increases blood flow to kidneys
  • Increases BP
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11
Q

Which 2 antioxidants are used in the prevention of AKI?

A
  1. Vitamin C: Decreases oxidation that is caused by free radicals
  2. Mucomyst:
    - Used as a mucolytic, antidote (APAP poisoning)
    - Some benefit in preventing contrast induced nephropathy in some patients
    - High sulfur content (rotten egg smell)
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12
Q

Treatment of AKI revolves around what?

A

Elimination of insult!
Reduce extra-renal complications
Expedite recovery

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13
Q

Name the treatments of AKI, we will then expand:

A

Dehydration, RRT, Pharmacologic therapy, Diuretics, Diuretic resistance, Electrolyte management

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14
Q

For dehydration, what 2 methods of tx are used?

A
  1. Oral therapy
  2. Isotonic IV fluids (20mL/kg) - smaller amount needed for oliguria/CHF

Goal: MAP > 65, urine output >0.5

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15
Q

Large volumes of NS can cause?

A

Hyperchloremic acidosis

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16
Q

What is RRT and what are the indications for it?

A

Renal replacement therapy

A,E,I,O,U:
Acid-base abnormalities
Electrolyte imbalance
Intoxications
Overload of fluid
Uremia
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17
Q

Pharmacologic Therapy for AKI, dosing considerations are?

A

Volume of distribution
Volume status of patient
Abx in septic patients

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18
Q

What is the main diuretic used in the tx of AKI?

A

Mannitol:

  • Osmotic diuretic
  • Can cause AKI itself, not used often
  • Must be filtered (can cause crystallization)
  • Used for head trauma, cerebral edema
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19
Q

When is the only time Loop diuretics are indicated for use in AKI?

A

Only for fluid overload

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20
Q

Loop diuretic resistance is common in AKI, why and what is done for this?

A

Increased dose doesn’t mean increased efficacy.

Switch oral to parenteral
Increase dose
Use continuous infusions
Use different agents

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21
Q

What are the causes of Diuretic resistance?

A
  • High sodium intake limits natriuretic effect
  • Patients with ATN have reduced number of working nephrons
  • Heavy proteinuria bind loop diuretics in renal tubule
  • Renal compensation at distal convoluted tubule
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22
Q

Which thiazides can be used in the case of loop diuretic resistance?

A

Chlorothiazide

Metolazone (good for renal pts)

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23
Q

Which agents at the collecting duct can be used for loop diuretic resistance?

A

Amiloride, Triamterene, Spirinolactone

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24
Q

During electrolyte management, how can hypernatremia and fluid retention be tx?

A

Limit sodium intake –> loop diuretic failure

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25
Q

During electrolyte management, how is hyperkalemia tx?

A

RRT

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26
Q

Which two elements are not removed by RRT effectively?

A

Phosphorus and Magnesium

Avoid calcium!

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27
Q

Pt’s on RRT can develop?

A

Hypocalcemia secondary to dialysis, need a Ca supplement

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28
Q

CKD

A

CKD

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29
Q

What are the initating factors of CKD?

A

DM
HTN
Glomerulonephritis

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30
Q

What happens in Anemia of CKD?

A

Decreased production of erythropoitetin (made in kidneys)

Iron deficiency common:
-Increased iron demands from erythropoietic stimulating agents (main cause for resistance)

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31
Q

CKD mineral and bone disorders are common in CKD populations due to abnormalities in?

A

PTH, Calcium, Phosphorus, Ca x P, Vitamin D

Renal osterodystrophy: kidneys can’t make vit. D

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32
Q

What happens in CKD Mineral and Bone disorder?

A

Decreased renal fxn –> Increased Phosphate –> Decreased Ca –> Increased PTH –> Increased Ca and P reabsorption

Decreased vit. D activation act. in kidney = Increased PTH

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33
Q

Management of CKD

A

Management of CKD

34
Q

Management of CKD: Nonpharm therapy

A

Diet: Limit protein/sodium

Smoking cessation and exercise

35
Q

Management of CKD: DM with CKD

A

ACEI or ARB to prevent further progression
-Titrated until GFR drops

Metformin should be continued until GFR < 30

36
Q

Management of CKD: HTN with CKD

A

Goal: <140/90
ACEI or ARB if pt with DM too
Thiazides not sufficient
Manage BP per other dz states

37
Q

Management of CKD: Anemia of CKD

A

ESA (Erythropoiesis stimulating agent)
Iron supplement

-Use Hgb for monitoring!

38
Q

When should ESA be discontinued? At what level of Hgb?

A

Above 10 - STOP!

39
Q

Increased mortality when Hb is kept above? (Black box warning)

A

13 g/dL

Still need iron supplements, can’t take ESA alone!

40
Q

What are the 2 examples of ESA?

A 
Epoetin alfa (Epogen, Procrit)
Darbepoetin alfa (Aranesp)
41
Q

Black box warnings of ESA:

A

Death, MI, Stroke, Cancer

42
Q

Management of CKD: Iron status

A

Required by CKD pt’s taking ESA’s

Should maintain adequate intake of Iron, B12, and folate

43
Q

Oral preps of Iron:

A

Ferrous sulfate
Ferrous gluconate
Ferrous fumarate

44
Q

Most common IV prep of iron:

A

Iron Sucrose (Venofer)

45
Q

Adverse effects of Iron:

A

Constipation
BLACKENED DISCOLORATION OF STOOL

IV forms:
Allergic rxns
Limited by slower infusions

46
Q

Management of CKD: Selecting an iron prep

A

Oral therapy 1st line if possible, fewer SE’s

IV for RRT pt’s

47
Q

Iron status while on ESA therapy monitored every?

A

3 months

48
Q

Tx goals for CKD Mineral and Bone disorder?

A

Keep calcium and phosphate in normal ranges
Ca x P < 55, otherwise indicative of dz

Monitor PTH

49
Q

CKD mineral and bone disorder: Non-pharm therapy?

A

Dietary phosphate reduction unless dialysis pt
Dialysis not sufficient enough
Parathyroidectomy if non-responsive to pharm tx’s

50
Q

CKD mineral and bone disorder: Phosphate binders

A

Binds to phosphate so it’s not absorbed

Tums
Calcium carbonate
Calcium acetate
Sevelamer
Alum hydroxide
51
Q

CKD mineral and bone disorder: What type of phosphate binder is better in early CKD? Why?

A

Calcium based are better in early CKD (pts are hypocalcemic)

Calcium carb soluble in acid, given before meals to bind Phosphate

52
Q

What is a nonabsorbable hydrogel that also lowers LDL and raises HDL?

A

Sevelamer

53
Q

AE’s of Phosphate binders:

A

Hypercalcemia, Aluminum toxicity

Drug-food, drug-drug interactions!
Calcium salts bind to oral meds (Iron, zinc, FQ’s)
separate agents

Aluminum toxicity will worsen anemia and can lead to CNS toxicity

54
Q

CKD mineral and bone disorder: Vitamin D therapy

A

Caclitriol is active 1,25 - D3
Suppresses PTH secretion, stimulates Ca absorption

Paricalcitol activate PTH receptors but don’t increase Ca and P absorption

55
Q

What does Cinacalcet (Sensipar) do?

A

Sensitizes PTH receptors to effects of Ca

Decreases PTH

56
Q

DRUG INDUCED KIDNEY INJURY

A

DRUG INDUCED KIDNEY INJURY

57
Q

Most common manifestation of DIKD?

A

Decreased GFR

58
Q

DIKD in 60% of hospital AKI?

A

Abx, NSAIDs, ACEIs, Anti-virals, chemo

59
Q

Signs of DIKD:

A

Decrease in GFR
Rise in Sir and BUN
“Dumb kidneys” not filtering effectively
Decreased urine output with HTN progression

60
Q

Proximal tubular injury:

A

metabolic acidosis

61
Q

Distal tubular injury:

A

Polyuria
Metabolic acidosis
Hyperkalemia

62
Q

DIKD structural/fxnal alterations: What drugs cause ATN?

A

aminoglycosides
Cisplatin, carboplatin
Cyclosporine, Tacrolimus

63
Q

DIKD structural/fxnal alterations: What drugs cause osmotic nephrosis?

A

Mannitol, IV immunoglobulin

Temporary injury

64
Q

DIKD structural/fxnal alterations: What drugs cause hemodynamically mediated kidney injury?

A

ACEI and ARB
NSAID
Changes in afferent/efferent arterioles

65
Q

DIKD structural/fxnal alterations: What drugs cause obstructive nephropathy?

Intratubular obstruction?
Nephrolithiasis?

A

Intratubular obstruction: Acyclovir, Methotrexate

Nephrolithiasis:
Sulfonamides
Anti-virals

66
Q

DIKD structural/fxnal alterations: What drugs cause Glomerular disease?

A

Lithium

NSAIDs

67
Q

DIKD structural/fxnal alterations: Vasculitis and thrombosis

A

Hydralazine
Allopurinol
Methamphetamines
Cyclosporine

68
Q

DIKD structural/fxnal alterations: Cholesterol emboli

A

Rare
Warfarin
Thrombolytics

69
Q

ATN

A

ATN

70
Q

Most common agents in ATN:

A 
Aminoglycosides
Contrast media
Cisplatin
Amphotericin B
Foscarnet
Osmotically active agents (Colloids, Manitol)
71
Q

ATN: Aminoglycosides

A

Gradually (5-10 days after therapy) progressive increase in BUN/SCr
Completely reversible

Damages cells

72
Q

ATN: Aminoglycosides Risk Factors

A

Large total dose
Prolonged therapy
Trough conc > 2
Concurrent nephrotoxins

73
Q

ATN: Aminoglycosides prevention

A

Alt. abx use
Limit concurrent nephrotoxin usage
Pharmacokinetic monitoring (change doses based on lvls)
Once daily dosing

74
Q

ATN: Radiographic Contrast Media Nephrotoxicity

A

Up to 50% of CKD pt’s
Oliguria in high-risk pts

Renal ischemia and direct cellular toxicity
High osmolarity

75
Q

ATN: Radiographic Contrast Media Nephrotoxicity Prevention

A

Contrast:

  • Minimize dose
  • Use non-iodinated contrast
  • Use low or iso-osmolar contrast

Avoid concurrent nephrotoxins

Sodium Bicarb (not really helpful) and Mucomyst

76
Q

ATN: Cisplatin Nephrotoxicity

A

Used for tumors

Major dose limiting toxicity: Nephrotoxicity

77
Q

ATN: Cisplatin Nephrotoxicity Prevention

A

Vigorous hydration with NS
Amifostine (Ethyol)
-Chelates cisplatin in cells

78
Q

ATN: Cisplatin Nephrotoxicity Tx

A

Partially reversible

Supportive care

79
Q

ATN: Amphotericin B Nephrotoxicity

A

Antifungal agent
Not common
Direct tubular cell damage

Prevention: Liposomal formulation (AmBisome)
Taking bilayer, embed in drug in bilayer –> no kidney damage inside

Tx: Supportive

80
Q

Intratubular Obstruction: Tumor lysis syndrome

A

Prevented by hydration and allopurinol

81
Q

Intratubular Obstruction: Rhabdo

A

HMG-CoA reductase inhibitors and CYP3A4 inhibitors

82
Q

Drugs that lead to AKI due to drug precipitation

A

Acyclovir, Foscarnet, Methotrexate

Clinical Pharmacology I (7 decks)

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