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SS- Renal > Drugs > Flashcards

Drugs Flashcards

1
Q

amphotercin B

A

nephrotoxic
pores in cell membrane and renal vasoconstriction
liposomal less toxic
Tx: volume expansion

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2
Q

VEGF inhibitors

A

nephrotoxic
interrupts fenestrated glomerular epithelium
results in HTN, proteinuria, thrombotic microangiopathy

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3
Q

EGFR inhibitors

A

nephrotoxic

hypomagnesemia and may inhibit P-gp

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4
Q

lithium

A

nephrotoxic
enters cell through ENaC
inhibits aquaporin 2 causing NDI

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5
Q

calcineurin inhibitors

A

nephrotoxic: difficult to tell in drug effect or transplant rejection

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6
Q

cisplatin

A

nephrotoxic and ototoxic
taken up by Ctr1 (copper) and OCT2
promotes cell death

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7
Q

calcium gluconate

A

IV: ~ 30 min
stabilizes membrane potential of myocardium
Tx: hyperkalemia

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8
Q

insulin

A

stimulates Na-H exchanger leading to a higher Na concentration to stimulate Na-K ATPase to take up K into cell
Tx: hyperkalemia

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9
Q

albuterol

A

Inhalation: B2 agonist
activates (phosphorylates) Na-K ATPase to take up K into cell
Tx: hyperkalemia

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10
Q

acetazolamide

A

PCT
carbonic anhydrase inhibitor: inhibits NaHCO3 reabsorption
effect: hyperchloremic systemic acidosis, alkaline urine, chloride reabsorption
Tx: glaucoma, cystinuria, seizure, mountain sickness

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11
Q

furosemide (Lasix)

A

loop diuretic
dilates veins: decrease LV filling pressure
SULFA drug
AE: ototoxicity, increase BUN, hyperglycemia, hyperuricemia, fluid and electrolyte imbalance, sialadentitis (inflammation of salivary glands)
DI: Lithium, indomethacin, probenecid, warfarin
secreted by organic acid transporter

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12
Q

bemtanide

A

loop diuretic
more POTENT than furosemide
useful with warfarin

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13
Q

torsemide

A

loop diuretic
vasodilator: lowers BP
longer T1/2

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14
Q

loop diuretics

A

block Na/K/2Cl transporter in TALH: high delivery of Na to distal nephron causing Na and H20 excretion
increase renal PG: increase RBF
stimulate renin release and maintain GFR
increase excretion: K, Ca, Mg, H (mild metabolic alkalosis)
Tx: edema, IV for acute pulmonary edema, hypercalcemia, protect against renal failure, washout toxins, HTN, SIADH
MOST POTENT diuretic
give NSAID to prevent resistance

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15
Q

thiazide diuretics

A

inhibit Na/Cl cotransporter in DCT: moderate Na/water excretion
Ca/Na counter transporter is more active: decrease Ca urinary excretion
increase Na to CD: increase K secretion
increase Mg excretion
Tx: edema, HTN, diabetes insipidus, hypercalciuria, osteoporosis, nephrogenic diabetes insipidus
AE: hypokalemia, hypomagnesia, hyperuricemia, hypercalcemia, hyperglycemia, lipid disorders, reduced GFR
GFR needs to be greater than 60 mL/min

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16
Q

K sparing diuretics

A 
inhibits Na reabsorption and K secretion
cortical collecting duct
decrease Na to CD: decrease K secretion
COMBINE with thiazides
AE: hyperkalemia, megaloblastic anemia in patients with cirrhosis
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17
Q

spirinolactone

A

aldosterone antagonist

AE: gynecomastia, hirsutism, uterine bleeding

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18
Q

amiloride

A

K sparing: ENac inhibitor

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19
Q

triamterene

A

K sparing: ENac inhibitor

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20
Q

kayexelate

A

K resin: removal of K in GI

Tx: hyperkalemia

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21
Q

eplernone

A

aldosterone antagonist

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22
Q

ethacrynic acid

A

loop diuretic

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23
Q

mannitol

A

osmotic diuretic

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24
Q

hydrochlorothiazide

A

thiazide

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25
Q

metolazone

A

POTENT thiazide

GFR greater than 30 needed

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26
Q

chlorthalidone

A

thiazide

long T1/2

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27
Q

quinothazone

A

POTENT thiazide

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28
Q

arginine vasopressin

A

ADH

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29
Q

desmopressin

A

ADH like drug

Tx: central diabetes insipidous, bleeding disorders, nocturnal enurisis

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30
Q

conivaptan

A 
IV
V2R antagonism
less selective for V2R than tolvaptan
Tx: hyponatremia
CYP3A4 metabolism
AE: numerous, infusion site rxn
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31
Q

tolvaptan

A

V2R antagonism
CYP3 metabolism
AE: hyplerglycemia, GI, clotting

32
Q

osmotic diuretic

A

inhibit Na/H2O reabsorption in PCT: decrease medullary tonicity impair ability of thin segments of LOH
increase excretion: urine, Na, K, Cl excretion
initially increase BP
Tx: dialysis disequilibrium syndrome, reduce intracranial and intraocular pressure
AE: volume overload
CI: cardiac failure

33
Q

aldosterone antagonist

A

late DT and CD
reduce ENac: increase Na excretion and reduce K
Tx: diuretic with thiazide, CHF, cirrhosis

34
Q

ADH like drug

A

V2R agonist
increase water permeability in CD
Tx: ADH-sensitive diabetes insidious, nephrogenic diabetes insipidous

35
Q

vaptans

A

VR2 antagonist

Tx: SIADH

36
Q

demeclocycline

A

V2R antagonist

Tx: SIADH

37
Q

terlipressin

A

IV; restricted use
V1R agonist: smooth muscle contration
Tx: ileus, reduce bleeding in esophageal varices and acute hemorrhagic gastritis

38
Q

renal cancer Tx in children

A

majority curable

classic cytotoxic agents in combination

39
Q

renal cancer Tx in adults

A

targeted drugs

TKI first, then mTOR inhibitor

40
Q

standard Wilm’s tumor or clear cell sarcoma in childrenTx

A

nephrectomy
radiation
vincristine, dactinomycin +/- doxorubicin
OR
vincristine, doxorubicin, cyclophosphamide, etoposide

41
Q

recurrent Wilm’s tumor Tx

A

alternate

  1. vincristine, doxorubicin, cyclophosphamide
  2. etoposide, cyclophosphamide
42
Q

recurrent clear cell sarcoma Tx in children

A

cyclophosphamide and carboplatin if not used initially
brain involvement: ICE: ifosfamide, carboplatin, etoposide
surgical resection and/or radiation

43
Q

Tx for rhabdoid and neuroepithelial tumor in children

A

none

44
Q

carboplatin

A

intrastrand DNA links

45
Q

cyclophosphamide

A

inter and intra-strand links

AE: hemorrhagic cystitis

46
Q

doxorubicin

A

intercalate, Topo-II inhibition, radicals

AE: cardiotoxic

47
Q

dactinomycin

A

intercalate, DNA dependent RNA synthesis inhibition; single strand breaks: free radical, topo-II
AE: hepatic dysfunction, extravasional necrosis

48
Q

etoposide

A

topo-II inhibitor

AE: hematologic, BP instability

49
Q

ifosfamide

A

inter and intrastrand links

AE: hemorrhagic cystitis

50
Q

vincristine

A

blocks tubulin polymerization

AE: peripheral neuropathy: “stocking glove”

51
Q

MESNA

A

give with cyclophosphamide

Tx hemorrhagic cystitis

52
Q

VEGF inhibitors

A 
clear cell renal carcinoma
bevacizumab
axitinib
sunitinib
sorafenib
pazopanib: EGFR inhibitor
all TKI: PDGFR inhibitor
AE: HTN
53
Q

mTOR inhibitors

A

bind FKBP12: inhibit immune, cell cycle, angiogenesis; promote apoptosis
Tx: clear cell renal carcinoma
CYP3A4 substrate
AE: maculopapular rash, mucosistis, anemia, fatigue, pulmonary infiltrates, blood dyscrasia

54
Q

-nib

A

oral
tyrosine kinase inhibitors
conserved ATP binding domain
resistance: ATP binding domain, and up regulation of mTOR2
metabolized by CYPs: CYP3A4
AE: hepatic, proteinuria
CV: HTN, QT, thromosis, hemorrhage, blood dyscrasia
endocrine: thyroid, adrenal, glucose need to monitor

55
Q

aldesleukin (IL-2)

A

T cell GF
activates JAK/STAT
AE: capillary leak syndrome (hypotension, tachycardia, hematoligic toxicity, pulmonary edema, renal toxicity); potential for sepsis
Tx: clear cell renal carcinoma

56
Q

IFN-alpha 2b

A

SC
activates JAK/STAT
AE: neuropsychiatric, infectious disorders, autoimmune, ischemic
less common AE: xerostomia, dysguesia, diaphoresis, cough, dizziness
Tx: clear cell renal carcinoma

57
Q

temsirolimus

A

mTOR inhibitor
IV weekly
metabolize to sirolimus

58
Q

everolimus

A

mTOR inhibitor

daily oral drug

59
Q

TKI with Steven Johnson syndrome

A

hypersensitivity
sorafenib
suntinib

60
Q

bevacizumab

A

IV infusion
VEGF inhibitor Ab
AE: thrombosis, HTN, CHF, proteinuria, blood dyscrasia, hemorrhage, GI perforation
WOUND HEALING complications

61
Q

renal cancer drugs that cause renal damage

A

carboplatin
ifosfomide
IL-2
targeted Tx not including mTOR inhibitors

62
Q

Drugs that induce hyperkalemia

A
  1. block Na channel in distal nephron: K sparing diuretics, trimethoprim, pentamidine
  2. block aldosterone production: ACEI/ARBs, NSAIDs, Heparin, tacrolimus
  3. block aldosterone receptors (spironolactone, eplerenone)
  4. block Na/K ATPase in distal nephron: cyclosporine
  5. extrarenal: digoxin, B2 blockers, somatostatin (inhibits insulin)
  6. K release from injured: tumor lysis syndrome, rhabdomyolysis, depolarizing paralytic agents
63
Q

drugs that induce hypokalemia

A

DIURETICS, ANTI-INFECTIVE agents

  1. increased excretion: diuretics, foscarnet, laxatives
  2. increased uptake: B2 agonist, dextrose, insulin, levothyroxine, theophylline
  3. misc: amphotericin B, caspofungin, corticosteroids, itrconazole
  4. 2 to hypomagnesemia: aminoglycosides, amphotericin B, cisplatin, cyclosporine, loop diuretics
64
Q

hypokalemia with low Mg

A

occludes ROMK channel
low Mg: K leaves cell and is excreted
MUST CORRECT to Tx hypokalemia

65
Q

NSAIDs (kidney injury)

A

AIN
inhibit PG: maintain adequate renal perfusion
chronic use: hyponatremia, hyperkalemia and metabolic acidosis, HTN

66
Q

ACEI/ARB (kidney injury)

A

inhibit renal auto-regulation of GFR
bilateral renal artery stenosis, volume depletion
hyperkalemia, acute renal injury

67
Q

aminoglycosides (kidney injury)

A

ATN
proximal tubule accumulation resulting in cell death
decrease K, Mg, Ca
accumulation in DT and CD can impair concentrating abilities
Tx: expand volume, limit dose

68
Q

SMX-TMP (kidney injury)

A

ATN, AIN
inhibits ENac; increased Cr without GFR effect
Tx: hydrate and alkalinize urine

69
Q

amphotericin B (kidney injury)

A

pores in cell membrane
renal tubular acidosis
renal vasoconstriction
tx: fluids

70
Q

VEGF inhibitors (kidney injury)

A

VEGF maintenance of fenestrated glomerular epithelium

HTN, proteinuria, thrombotic microangiopathy

71
Q

EGFR Ab (kidney injury)

A

cetuximab
hypomagnesemia
inhibit P-gp

72
Q

lithium (kidney injury)

A

ENac

dysregulation of AQP-2 and develop NDI

73
Q

calcineurin inhibitors (kidney injury)

A

cyclosporine, tacrolimus
interstitial fibrosis
inhibit transfer of NF-AT to nucleus

74
Q

cisplatin (kidney injury)

A

ATN
promote cell death
TNF-alpha production in tubular cells

75
Q

acute interstitial nephritis (AIN)

A 
onset: 10-14 d 
Sx: fever, rash, eosinophilia
UA: WBC casts, hematuria, proteinuria, eosinophiluria
Tx: stop drug, corticosteroids
Dx: biopsy
76
Q

acute tubular necrosis (ATN)

A 
onset: 7-10 d
uremic Sx
UA: granular casts, renal epithelial cast, oliguria
Dx: Hx, exam, labs
initiation, maintenance, recovery
proximal straight tubule, TALH
hypoprefusion + casts and debris collect in tubule; ATP depleted
Tx: discontinue
contrast

SS- Renal (11 decks)

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