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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
During electrolyte management, how is hyperkalemia tx?
RRT
26
Which two elements are not removed by RRT effectively?
Phosphorus and Magnesium Avoid calcium!
27
Pt's on RRT can develop?
Hypocalcemia secondary to dialysis, need a Ca supplement
28
CKD
CKD
29
What are the initating factors of CKD?
DM HTN Glomerulonephritis
30
What happens in Anemia of CKD?
Decreased production of erythropoitetin (made in kidneys) Iron deficiency common: -Increased iron demands from erythropoietic stimulating agents (main cause for resistance)
31
CKD mineral and bone disorders are common in CKD populations due to abnormalities in?
PTH, Calcium, Phosphorus, Ca x P, Vitamin D | Renal osterodystrophy: kidneys can't make vit. D
32
What happens in CKD Mineral and Bone disorder?
Decreased renal fxn --> Increased Phosphate --> Decreased Ca --> Increased PTH --> Increased Ca and P reabsorption Decreased vit. D activation act. in kidney = Increased PTH
33
Management of CKD
Management of CKD
34
Management of CKD: Nonpharm therapy
Diet: Limit protein/sodium | Smoking cessation and exercise
35
Management of CKD: DM with CKD
ACEI or ARB to prevent further progression -Titrated until GFR drops Metformin should be continued until GFR < 30
36
Management of CKD: HTN with CKD
Goal: <140/90 ACEI or ARB if pt with DM too Thiazides not sufficient Manage BP per other dz states
37
Management of CKD: Anemia of CKD
ESA (Erythropoiesis stimulating agent) Iron supplement -Use Hgb for monitoring!
38
When should ESA be discontinued? At what level of Hgb?
Above 10 - STOP!
39
Increased mortality when Hb is kept above? (Black box warning)
13 g/dL Still need iron supplements, can't take ESA alone!
40
What are the 2 examples of ESA?
``` Epoetin alfa (Epogen, Procrit) Darbepoetin alfa (Aranesp) ```
41
Black box warnings of ESA:
Death, MI, Stroke, Cancer
42
Management of CKD: Iron status
Required by CKD pt's taking ESA's | Should maintain adequate intake of Iron, B12, and folate
43
Oral preps of Iron:
Ferrous sulfate Ferrous gluconate Ferrous fumarate
44
Most common IV prep of iron:
Iron Sucrose (Venofer)
45
Adverse effects of Iron:
Constipation BLACKENED DISCOLORATION OF STOOL IV forms: Allergic rxns Limited by slower infusions
46
Management of CKD: Selecting an iron prep
Oral therapy 1st line if possible, fewer SE's | IV for RRT pt's
47
Iron status while on ESA therapy monitored every?
3 months
48
Tx goals for CKD Mineral and Bone disorder?
Keep calcium and phosphate in normal ranges Ca x P < 55, otherwise indicative of dz Monitor PTH
49
CKD mineral and bone disorder: Non-pharm therapy?
Dietary phosphate reduction unless dialysis pt Dialysis not sufficient enough Parathyroidectomy if non-responsive to pharm tx's
50
CKD mineral and bone disorder: Phosphate binders
Binds to phosphate so it's not absorbed ``` Tums Calcium carbonate Calcium acetate Sevelamer Alum hydroxide ```
51
CKD mineral and bone disorder: What type of phosphate binder is better in early CKD? Why?
Calcium based are better in early CKD (pts are hypocalcemic) Calcium carb soluble in acid, given before meals to bind Phosphate
52
What is a nonabsorbable hydrogel that also lowers LDL and raises HDL?
Sevelamer
53
AE's of Phosphate binders:
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
CKD mineral and bone disorder: Vitamin D therapy
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
What does Cinacalcet (Sensipar) do?
Sensitizes PTH receptors to effects of Ca | Decreases PTH
56
DRUG INDUCED KIDNEY INJURY
DRUG INDUCED KIDNEY INJURY
57
Most common manifestation of DIKD?
Decreased GFR
58
DIKD in 60% of hospital AKI?
Abx, NSAIDs, ACEIs, Anti-virals, chemo
59
Signs of DIKD:
Decrease in GFR Rise in Sir and BUN "Dumb kidneys" not filtering effectively Decreased urine output with HTN progression
60
Proximal tubular injury:
metabolic acidosis
61
Distal tubular injury:
Polyuria Metabolic acidosis Hyperkalemia
62
DIKD structural/fxnal alterations: What drugs cause ATN?
aminoglycosides Cisplatin, carboplatin Cyclosporine, Tacrolimus
63
DIKD structural/fxnal alterations: What drugs cause osmotic nephrosis?
Mannitol, IV immunoglobulin | Temporary injury
64
DIKD structural/fxnal alterations: What drugs cause hemodynamically mediated kidney injury?
ACEI and ARB NSAID Changes in afferent/efferent arterioles
65
DIKD structural/fxnal alterations: What drugs cause obstructive nephropathy? Intratubular obstruction? Nephrolithiasis?
Intratubular obstruction: Acyclovir, Methotrexate Nephrolithiasis: Sulfonamides Anti-virals
66
DIKD structural/fxnal alterations: What drugs cause Glomerular disease?
Lithium | NSAIDs
67
DIKD structural/fxnal alterations: Vasculitis and thrombosis
Hydralazine Allopurinol Methamphetamines Cyclosporine
68
DIKD structural/fxnal alterations: Cholesterol emboli
Rare Warfarin Thrombolytics
69
ATN
ATN
70
Most common agents in ATN:
``` Aminoglycosides Contrast media Cisplatin Amphotericin B Foscarnet Osmotically active agents (Colloids, Manitol) ```
71
ATN: Aminoglycosides
Gradually (5-10 days after therapy) progressive increase in BUN/SCr Completely reversible Damages cells
72
ATN: Aminoglycosides Risk Factors
Large total dose Prolonged therapy Trough conc > 2 Concurrent nephrotoxins
73
ATN: Aminoglycosides prevention
Alt. abx use Limit concurrent nephrotoxin usage Pharmacokinetic monitoring (change doses based on lvls) Once daily dosing
74
ATN: Radiographic Contrast Media Nephrotoxicity
Up to 50% of CKD pt's Oliguria in high-risk pts Renal ischemia and direct cellular toxicity High osmolarity
75
ATN: Radiographic Contrast Media Nephrotoxicity Prevention
Contrast: - Minimize dose - Use non-iodinated contrast - Use low or iso-osmolar contrast Avoid concurrent nephrotoxins Sodium Bicarb (not really helpful) and Mucomyst
76
ATN: Cisplatin Nephrotoxicity
Used for tumors | Major dose limiting toxicity: Nephrotoxicity
77
ATN: Cisplatin Nephrotoxicity Prevention
Vigorous hydration with NS Amifostine (Ethyol) -Chelates cisplatin in cells
78
ATN: Cisplatin Nephrotoxicity Tx
Partially reversible | Supportive care
79
ATN: Amphotericin B Nephrotoxicity
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
Intratubular Obstruction: Tumor lysis syndrome
Prevented by hydration and allopurinol
81
Intratubular Obstruction: Rhabdo
HMG-CoA reductase inhibitors and CYP3A4 inhibitors
82
Drugs that lead to AKI due to drug precipitation
Acyclovir, Foscarnet, Methotrexate

Clinical Pharmacology I (7 decks)

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