Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
40 Cards in this Set
- Front
- Back
People with renal insufficiency should avoid which type of drugs?
|
NSAIDs and COX-2 inhibitors
|
|
What is the MOA and toxicity of Nitrofurantoin?
|
Bactericidal, damages bacterial DNA. It is nephrotoxic, can cause diabetes insipidus
|
|
What is the MOA of pentamidine? Toxicity?
|
treats pneumonia caused by pneumocystis carini. Nephrotoxic
|
|
What are the antihyperlipidemics? And what is their MOA
|
Lovestatin and Gemfibrozil. Lovestatin inhibits HMG CoA reductase. Gemfibrozil upregulates lipoprotein lipase (LPL) synthesis and increases oxidation of fatty acids
|
|
What is the nephrotoxic effect of the antihyperlipidemics?
|
Rhabdomyolysis, muscle injury (myopathy), possible myoglobinuria and renal damage
|
|
Which drugs of the ACEIs and ARBs are nephrotoxic? And what is their nephrotoxic effect?
|
Losartan and Captopril. Hypotension, renal failure, and hyperkalemia
|
|
Which of the drugs of the Diuretics are nephrotoxic?
|
Furosemide, Hydrochlorothiazide, Triamterene, and Mannitol
|
|
What is MESNA? What drugs is it used with?
|
sulfhydryl that inactivates acrolein which is the nephrotoxic metabolite in ifosphamide and cyclophosphamide
|
|
What two drugs of the chemotherapy drugs are alkylating agents?
|
Cisplatin and Mitomycin
|
|
What is the MOA of cisplatin?
|
Chemotherapy. Complexes with DNA forming intrastrand and interstrand crosslinks of guanine.
|
|
What is the mechanism of toxicity of cisplatin?
|
conversion of nephrotoxin in proximal tubules. Results in hypomagnesium, hyokalemia, hypocalcemia, hyponatremia, hypophosphatemia and hyperurecemia
|
|
What drug causes severe nephropathy and inhibits dihydrofolate reductase (DHFR)
|
Methotrexate, chemotherapy drug
|
|
What drug can cause microangiopathic hemolytic anemia, and if combined with thrombocytopenia and irreversible renal failure cause Hemolytic Uremic Syndrome?
|
Mitomycin, a chemotherapy drug
|
|
What are the cyclosporines and what is their MOA?
|
(chemotherapy) Tacrolimus and Immunosuppressine. Block activation of T cells in early stage of differentiation
|
|
What is the nephrotoxicity of the Cyclosporines (tacrolimus FK-506 and immunosuppressine)
|
Hemodynamic factors- vasoconstriction via the sympathetic system. Results in renal ischemia
|
|
What is the MOA of ifosphamide and cyclophosphamide?
|
DNA intrastrand and interstrand cross link at N7 of guanine
|
|
What is the nephrotoxicity of ifosphamide and cyclophosphamide?
|
Hemorrhagic cyctitis and hematuria, Acute tubular necrosis and Fanconi Syndrome- require MESNA
|
|
How can nephrotocity be avoided when using cisplatin?
|
adequate hydration and dilute drug in saline
|
|
How can nephrotoxicity be avoided in methotrexate
|
if patient is receiving a high dose, give large volume parenterals (LVP) of Na Bicarbonate in to increase elimination
|
|
How can nephrotoxicity be avoided when using mitomycin?
|
plasma exchange corrects the hemolytic anemia
|
|
In what class of people would NSAIDs and COX-2 inhibitors cause renal failure and how?
|
Compromised patients (CHF, cirrhosis, nephrosis). These patients already have overexpressed COX-2 so NSAIDs and COX-2Is block compensatory vasodilation so maintanence of Renal Blood Flow and GFR are lost => acute renal failure
|
|
Which hormones increase GFR
|
NO and prostoglandins
|
|
What hormones decrease GFR
|
Norepi, Epi, endothelin
|
|
What is the nephrotoxity of lithium?
|
Nephrogenic Diabetes Insipidus, from the downregulation of V2, a vasopressin regulated channel on the apical membrane of the collecting duct
|
|
which drug can be used to avoid Diabetes insipidus in the use of lithium?
|
Desmopressin
|
|
What is the nephrotoxicity of laxatives, how can you avoid?
|
diffuse tubular injury and abundant deposits of Ca phosphate in Distal and collecting ducts. Causes volume depletion and hypokalemia. Treatment: hydration
|
|
What is the mechanism of toxicity of contrast nephropathy?
|
causes acute tubular necrosis by direct vasoconstriction by contrast agent and generation of free radicals toxic to glomeruli and tubules
|
|
How can contrast nephropathy toxicity be avoided?
|
Low dose and isomola, avoid NSAIDs. Drug options: anti-diabetic Metformin, acetylcysteine, large volume parenteral of Na bicarb
|
|
Nitroglycerin (class and other drugs)
|
Nitrates w/ Amyl nitrate, isosorbide dinitrate, isosorbide mononitrate
|
|
Sildenafil (class and other drugs)
|
5-phosphodiesterase inhibitors w/ Tadalafil, Vardenafil
|
|
What is the MOA of the 5-PDEI?
|
increase concentration of cGMP by blocking the degradation of 5-PDE, which line the smooth muscle cells of the blood vessels in the corpus cavernosum
|
|
What class of drugs should be avoided when using 5-PDEIs?
|
Nitrates
|
|
What is the MOA of nitroglycerin?
|
NO activates cGMP to cause dephos of myosin light chain to stop smooth muscle contraction => vasodilates, ateriodilates, and relaxes other smooth muscle
|
|
What anginas can nitrates be used for?
|
Typical and Atypical
|
|
Which of the nitrates are oral? Inhaled?
|
isosorbide mononitrate and dinatrate (sublingual too), nitroglycerin (subling). Inhaled- amyl nitrate
|
|
What is the toxicity of nitrates?
|
hypotension, fainting, pulsing headache
|
|
What are the short-acting nitrates
|
nitroglycerin, isosorbide dinitrate, amyl nitrate
|
|
What are the long acting nitrates
|
nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
|
|
What drugs potentiate the natural NO mechanism
|
5-PDE
|
|
What is the drug toxicity when using a nitrate and a 5-PDEI?
|
Severe hypotension, reflexive tachycardia, V. contractility, cardiac ischemia, anginal pain, MI
|