03a: Pharmacology Renal Drugs Flashcards Preview

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Flashcards in 03a: Pharmacology Renal Drugs Deck (49)
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1
Q

T/F: ACEi/ARBs are prescribed to all diabetic patients to prevent nephropathy.

A

False - not in normotensive patients (only if HTive)

2
Q

Diabetic patients should be screened for signs of nephropathy. How is this done?

A

Testing urine albumin levels

3
Q

T/F: ACEi /ARBs affect mesangial cells.

A

True - inhibit AII-induced mesangial cell growth/matrix deposition

4
Q

Central DI is treated with (X) drug, (selective/non-selective) for (Y).

A

X = desmopressin
Selective
Y = V2

5
Q

How is desmopressin administered?

A

Oral or nasal

6
Q

Nephrogenic DI is treated with (X) drug(s). What’s the mechanism?

A

X = diuretics (thiazides, amiloride)

Induce diuresis (counter-intuitive) but then V depletion enhances water absorption in proximal tubule

7
Q

It’s important for nephrogenic DI patient to be on (X) diet.

A

X = low Na, low protein

8
Q

What are the indications to use immunosuppressive drugs for renal disease?

A
  1. Type II or III HS reactions in kidney

2. Transplant (rejection prevention/treatment)

9
Q

List the three mechanisms (classes) of immunosuppressives used for renal diseases.

A
  1. Ab against T-cell membrane Ag
  2. B/T cell replication inhibitors
  3. Intracellular T-cell signaling inhibition
10
Q

Basiliximab structure and mechanism.

A

Anti-IL2 receptor monoclonal Ab;

Selective binding to CD25 on T cells

11
Q

You prescribe your kidney transplant patient an Ab immunosuppressive that depletes T cells. He develops fever, chills, and hypotension due to (X) release. Which drug is responsible for this?

A

X = cytokine

Antithymocyte globulin (rabbit ATG)

12
Q

T/F: Basiliximab causes T-cell depletion without cytokine release/side effects of antithymocyte globulin.

A

False - causes neither

13
Q

Purine antimetabolite drugs cause side effects primarily due to:

A

Their inhibition of cell replication in other sites (non-target tissue)

14
Q

(X) immunosuppressant is administered as prodrug, which is then converted to active carboxylate form, (Y). This drug is a very efficacious selective inhibitor of IMP dehydrogenase. Which class of drugs does this fall under?

A
X = mycophenolate mofetil
Y = mycophenolate

Purine antimetabolites

15
Q

Calcineurin inhibitors block which (X)-mediated action?

A

X = calcineurin

dephosphorylation of cytosolic transcription factors

16
Q

The end result of calcineurin inhibitor action is to (up/down)-regulate (X) (transcription/translation/replication).

A

Down;
X = IL2
Transcription

17
Q

List the drugs that are calcineurin inhibitors. Star the one with lower risk of side effects.

A
  1. Cyclophosphamide

2. Tacrolimus*

18
Q

List potential side effects of calcineurin inhibitors.

A
  1. HT, hyperlipidemia
  2. Diabetes
  3. Neuro
  4. Nephrotoxicity!!!
19
Q

It’s important to monitor drug levels of (mycophenolate/tacrolimus/basiliximab) in patient that’s slow CYP inducer.

A

Tacrolimus

20
Q

Kidney transplant patient on (X) immunosuppressant presents with nephrotoxic decrease in GFR. What are the drug’s mechanisms for nephrotoxicity?

A

X = calcineurin inhibitor (cyclophosphamide, tacrolimus)

  1. Afferent arteriole constriction and obliterative vascular pathology
  2. Tubular vacuolization/atrophy
  3. Interstitial fibrosis
21
Q

Sirolimus, aka (X) is (agonist/antagonist) of (Y).

A

X = rapamycin
Antagonist
Y = mTOR (“target of rapamycin”)

22
Q

(X) immunosuppressant drug blocks mTOR activity, which is required for (Y).

A
X = sirolimus/rapamycin
Y = cytokine-mediated shift from G1 to S phase in cell cycle
23
Q

End result of rapamycin/sirolimus action is (stimulation/inhibition) of (X)-mediated activation of (Y) cells.

A

Inhibition
Y = IL-2
Y = B/T Cells

24
Q

Sirolimus is (more/less) efficacious and (more/less) nephrotoxic than cyclophosphamide.

A

Less, less (though may be new warnings of nephrotoxicity)

25
Q

Current drug protocols for renal transplant patients: induction with (X) drugs and then pre-adaptation with (Y) drugs.

A

X = anti-thymocyte globulin (ATG) or anti-CD25 Ab (IV)

Y = Combo PO Rx (calcineurin inhibitors, mycophenolate mofetil, prednisone)

26
Q

Current drug protocols for renal transplant patients: post-adaptation regimen involves (mono/combo)-Rx with:

A

Combo; same drugs as pre-adaptation (calcineurin inhibitors, mycophenolate mofetil, prednisone), but lower doses
Taper off steroids

27
Q

List four classes/examples of nephrotoxic drugs that cause ATN.

A
  1. Dyes/radioconstrast agents
  2. Chemotherapeutics (cisplatin)
  3. Aminoglycosides (gentamicin)
  4. Amphotericin B
28
Q

Gentamicin has clearance most similar to (PAH/Creatinine/Inulin/Glucose/Urea).

A

Creatinine;

Over 90% eliminated by kidney BTW

29
Q

Patients taking acetaminophen are at risk for nephrotoxicity. Specifically, which pathological changes?

A
  1. Chronic interstitial nephritis
  2. Papillary necrosis/calcification

Increase risk of ESRD

30
Q

T/F: Analgesic nephropathy is dose-dependent.

A

True

31
Q

NSAID/COX2i nephrotoxicity is related to their effect of (increase/decrease) in (X) synthesis.

A

Decrease;

X = Prostaglandin

32
Q

You would be concerned about analgesic nephrotoxicity in patient with which risk factors?

A
  1. Age
  2. HT, diabetes
  3. Renal impairment
  4. On diuretics
33
Q

List two examples of drugs/classes that have been shown to induce crystalluria.

A
  1. Sulfa antibiotics (ex: sulfadiazine)

2. Acyclovir (prodrug is valacyclovir)

34
Q

Ethanol and (X) drug both (stimulate/inhibit) vasopressin actions. They do this by (similar/different) mechanism(s).

A

X = Li
Inhibit
Different (EtOH blocks ADH release from pituitary and Li blocks signaling via V2-R)

35
Q

Lithium effect on (X) in distal tubule typically causes (diuresis/retention). What can be given to prevent this?

A

X = V2 receptor
Diuresis

Amiloride (ENaC blocker) - prevents Li uptake into tubular cell

36
Q

List three drugs/classes that induce SIADH.

A
  1. Oral hypoglycemics
  2. Antineoplastics
  3. Psychoactive drugs
37
Q

SIADH Treatment:

A
  1. Saline (correct serum Na)
  2. Furosemide (decrease medullary hypertonicity)
  3. V2-R antagonist
38
Q

“-vaptan” drugs, such as conivaptan, have which action?

A

V2-R antagonists

39
Q

What are the reasons behind reduction in ‘Nonrenal’

Clearance of a drug in Renal Disease?

A
  1. Impaired biotransformation by kidney

2. Impaired hepatic clearance (uremic toxins downregulate CYP and decrease oatp-mediated hepatic drug uptake)

40
Q

For patients with renal impairment, use an opioid (with/without) (X).

A

Without;
X = an active metabolite

(if metabolite accumulates due to poor clearance, will have additional opioid effects)

41
Q

(Codeine/fentanyl/morphine) is/are preferred opioids in patients with renal impairment.

A

Fentanyl (inactive metabolite)

Codeine and morphine active metabolite (morphine-6-glucuronide) has opioid effects and is cleared by kidney

42
Q

Trimethoprim/sulfamethoxazole are used for (X) renal disease. Dose should be reduced by 50% if GFR is (Y) mL/min.

A
X = UTI (antibacterials)
Y = 15-30
43
Q

Trimethoprim/sulfamethoxazole are contraindicated in patients with GFR of (X) mL/min.

A

X = under 15

44
Q

Dose adjustment for quinolones is required in patients with GFR of (X) mL/min.

A

X = under 50

45
Q

Normal saline contains (X) mEq/L of Na and (Y) mEq/L of Cl. Thus, total osmolality is (Z) mEq/L.

A
X = Y = 154
Z = 308
46
Q

Free Water Excess/Deficit equation:

A

0.6xTBWx(1-(serum Na/140))

47
Q

Adrogue formula allows you to calculate (X). What’s the formula?

A

X = how much serum Na will drop with 1 L of IVF

Infusate Na - serum Na)/(TBW+1

48
Q

When you give patient D5W/hypotonic fluid, (ECF/ICF) V rises.

A

Both BUT ICF more (most of the fluid will go into the cells - so if you give 1.5 L, 1 L to ICF, 0.5 L to ECF)

49
Q

IVF in patient with SIADH and serum Na of 110 mEq/L should be given (X)% normal saline, which has osmolality of (Y) mOsm/L.

A
X = 3 (hypertonic)
Y = 900