Exam 4 Flashcards
Most common manifestation of drug induced kidney disease?
Decline in GFR
Rise in serum creatinine and blood urea nitrogen (BUN)
GFR/blood volume are opposite to BUN
MC lab abnormalities of drug induced kidney disease
Increase in Scr of >0.3mg/dL in 48 hours OR Increase in Scr of 1.5x baseline OR Reduced urine output (<0.5mL/kg/h for more than 6 hours
Drugs involved in acute tubular necrosis
Aminoglycosides, contrast dye, chemo drugs (cisplatin), amphotericin, cyclosporin
Drug classes involved in hemodynamically mediated kidney injury
NSAIDs, ACEs, ARB, cyclosporine
What kind of kidney injury do sulfonamides and NSAIDs cause?
Prerenal, vasculitis, nephrotic syndromes, obstructions, acute interstitial nephritis
What classes of meds cause acute allergic interstitial nephritis?
Penicillins, cipro, NSAID/Cox2s, Proton pump inhibitors, loop diuretics (furosemide)
What type of kidney injury does hydralazine/methamphetamines cause?
Vasculitis and thrombosis
What type of kidney injury does warfarin cause?
Cholesterol emboli
Risk Factors of Contrast Induced Nephrotoxicity
GFR <60, decreased renal blood flow, concurrent nephrotoxins (NSAIDs/ACE)
Prevention/Monitoring of CIN
Alternate imaging, hydration and antioxidants
Monitor renal function (LFTs), electrolytes and volume status
Amphotericin Nephrotoxicity
Reduced renal blood flow exacerbating ischemia, may be irreversible
Decreased GFR, ^Scr/BUN
Wasting of potassium, sodium and magnesium
Prevention of Amphotericin B Nephrotoxicity
Switch from liposomal form in high risk, increase infusion time, alternate antifungals (azaleas, caspofungin)
Monitor LFTs and electrolytes
ACE/ARB Nephrotoxicity
Reduced renal blood flow (>efferent and small afferent)
Decreased urine output, Scr rise of >30% in 3-5 days, stabilizes in 1-2 week (reversible)
Prevention/Management of ACE/ARB Nephrotoxicity
Choose shorter acting drugs (prils)
Low doses/titration
Discontinue if Scr increases >30%, can attempt to restart after correcting volume depletion
NSAID/Cox-2 Nephrotoxicity
Renal ischemia/reduced GFR from inhibited vasodilation (constricted afferent)
Diminished urine output, weight gain/edema, Scr/BUN/potassium/BP all elevated
Prevention of NSAID/Cox2 Nephrotoxicity
Avoid potent compounds (indomethacin for gout), use analgesics witless PGE inhibition (acetaminophen), use shorter half-lives
Crystal Nephropathy Causes
Precipitation of drug crystals in tubular lumen from hyperuricemia (treat w/ hydration and allopurinol), Rhabdomyolysis (treat with statins; increased risk with CYP3A4 drugs)
What is the leading cause of CKD?
Diabetes
Diabetes Treatment in CKD
ACE or ARB if urine albumin >30mg/24h
dose is increased until a drop in GFR, hyperkalemia or albuminuria reduced by 30-50%
Hypertension Treatment in CKD
ACE or ARB, if albuminuria is down butBP is still high, increase dose or dd thiazide or dihydropyridine Second lines (for pregnant): nondihydros (diltiazem, verapamil) or alosdterones (spironolactone)
Anemia Treatment in CKD
ESAs and iron supplementation
Anemia Monitoring
Reticulocytes
Erythropoetin Stimulating Agents Mechanism of Action
Stimulates division of differentiation of committed erythroid progenitor cells, induces release of reticulocytes from bone marrow into blood
Short (epoetin) and long (darbepoetin) acting version
Erythropoetin Stimulating Agents AEs
Box warning: increased CV and CKD events with Hg>11
Cancer (shortened survival when Hg >12), increased risk of DVT
What is the treatment goal in anemia?
Hb change of 1-2g/dL in 4 weeks
PTH, vitamin D and FGF23 effects on serum calcium/phosphate levels
PTH: increased calcium, decreased phosphate
Vit D: Increased calcium and phosphate
FGF23: decreased phosphate
Mineral/bone Disorder management
Dietary phosphorus restriction (pumpkin seeds, edamame, bacon, bakers yeast), phosphate binding agents, vit D supplementation and calcimimetic therapy
Calcium based phosphate binders MOA
forms insoluble calcium phosphate to be excreted in feces
Calcium based phosphate binders Indications and AEs
CKD hyperphosphatemia
AEs: milk-alkali syndrome (HA, nausea, irritability, weakness, hypercalciumia)
Types of Calcium based phosphate binders
Calciumacetate, calcium carbonate (tums)
Types of Resin Binders
Sevelamer carbone, sevelamer hydrochloride
Sevelamer Hydrochloride MOA
Binds phosphate within intestinal lumen limiting absorption and decreased serum phosphate concentrations
Sevelamer Hydrochloride Indications/AEs
Indications: Risk of extraskeletal calcification, hyperphosphatemia, high LDL
AEs: metabolic acidosis, N/V/D and dyspepsia
Lanthanum Carbonate MOA
Binds dietary phosphate>insoluble lanthanum phosphate complexes with decreases in phosphate and calcium levels
Lanthanum Carbonate Indications/AEs
Hyperphosphatemia
AEs: bowel obstruction, constipation, dyspepsia, fecal impaction, ileus
Aluminum Hydroxide MOA
Binds phosphate in GI tract preventing phosphate absorption
Aluminum Hydroxide Indications/AEs
NOT FIRST LINE; short term use for hyperphosphatemia with no response to other binders
AEs: aluminum toxicity, constiption, fecal impaction, hypomagnesemia, hypophosphatemia
Ergocalciferol and Cholecalciferol D2 MOA
Stimulates calcium and phosphate absorption in small intestine, promotes secretion of calcium from bone to blood, promotes renal tubule phosphate reabsorption
Ergocalciferol and cholecalciferol Indications and AEs
Hypophosphatemi, hypoparathyroidism
AE: hypercalcemia
Calcitrol
Used for hypocalcemia in pts on chronic renal dialysis
Types of ESAs
Epoetin alpha (short half life), darbepoetin alpha (long half-life), methoxy PEG-epoetin beta (really long half life) all available IV or subQ
ESA Initiation in CKD Anemia
Do not start if Hb>10 (best between 9-10)
Hb Levels in CKD Anemia
Do not use ESAs to intentionally increase >13 or to maintain >11.5
Iron Initiation in CKD Anemia
Start when Transferrin saturation <30% and ferritin is <500
Goals of UTI Treatment
Eradicate invading organism, prevent/treat consequences of infection, prevent recurrence of infection, decrease potential for collateral damage with too broad therapy
Microbes Associated with UTIs
E. coli #1
Staph saprophytic, klebsiella, proteus spp, pseudomonas, enterococcus
Recommended Treatment for Uncomplicated UTI
3 days of bactrim, 1 dose of fosftomycin or 5 days nitrofurantoin
Recommended Treatment of Pyelonephritis/Complicated UTIs
3 days of Cipro, levofloxacin
Bactrim MOA/Comments
Inhibits Folate Synthesis
Effective against aerobes except P. aeruginosa, effective prophylaxis
Nitrofurantoin MOA/Comments
Advantage is a lack of resistance
Can be used in pregnancy but can cause hemolytic anemia when close to delivery
Cipro/levofloxacin MOA/Comments
Inhibits DNA Gyrase
Cover P aeruginosa, Avoid in kids/pregnancy
Cipro>levo
Fosfomycin MOA
Inhibits cell wall synthesis
Beta-lactam MOA
Penicillins/cephalosporins (augmenten is preferred)
Inhibits cell wall synthesis
Bactrim AEs/Monitoring
AEs: rash, stevns-johnson, renal failure, photosensitivity
Monitor Scr, BUN, electrolytes, CBC
Nitro AEs/monitoring
GI intolerance, neuropathies, pulmonary reactions
Monitor Scr and BUN
Fluoroquinolone (Cipro/levo) AEs/Monitoring
Hypersensitivity, photosensitivity, GI symptoms, dizziness, confusion, tendonitis
Monitor CBC, Scr, BUN
Penicillin AE/Monitoring
Hypersensitivity (rash, anaphylaxis), diarrhea, seizure
Monitor CBC, signs of rash/hypersensitivity
Treatment of uncomplicated cystitis
1: nitro x5days bactrim x3 days fosfomycin x1 dose fluoroquinolone x3 days blactams x3-7 days
Treatment of Cystitis in Pregnancy
Augmentin x7 days
cephalosporin x7 days
bactrim x7 days
Treatment of Uncomplicated pyelonephritis
Quinolone x7 days
bactrim x14 days
augmenter x 14 days if gram positive
Treatment of Complicated Pyelonephritis
Quinolone x14 days
Prostatitis Treatment
Bactrim x4-6 weeks
Quinolone x 4-6 weeks
Cranberry Juice in UTI
Decreases adherence of bacteria to bladder epithelial cells
Phenazopyridine HCl
Azo-dye
Can mask a worsening UTI
Colors body fluids red-orange/can’t wear contacts bc of this
Dose restricted max 200 mg TID for 1-2 days
UTI in Pregnancy
Treat whether symptomatic or not
Cephalexin, amoxicillin or augmente for 5-7 days
Principles of Topical Term Therapy
Efficacy of a topical drug depends on its inherent potency and its ability to penetrate the skin
Factors that affect this are: concentration, thickness/integrity of corneal, frequency of application, occlusiveness of vehicle and compliance
Regional Penetration Levels
Mucus membrane>scrotum>eyelids>face>chest/back>
upper arms/legs>lower arms/legs>doors of hands/feet>palmar and plantar skin>nails
Goals of Derm Treatment
Counteract disease, reduce inflammation, relieve symptoms, promote epithelial healing, restore cutaneous integrity, prevent complications
Types of Term Treatments
Cleansing agents, absorbent dressings/powders, anti-inflammatory, anti-infective, astringents, drying agents, moisturizing agents, keratolytics, antipruritics
Types of Term Vehicles
Liquid/oil combos (ointment or cream), liquids (lotion, foam, gel, solution, soaks/baths), spray, powder
How to determine quantity of topical treatments
Rule of 9’s
1 palm area =1% body surface (2 palms BID requires 30 g for 1 month)
Fingertip Units for steroids (2 fingertips=1g=4 palms)-apply sparingly!
How can you enhance absorption of topical treatment?
Occlusion!-plastic wrap, cotton socks, nylon suit, waterproof dressing
Types of dressings
Nonocclusive (gauze)
Wet-to-dry (wetted in saline, allowed to evaporate)
Occlusive (increases absorption and effectiveness; hydrocolloid can just use gauze)
Corticosteroids in Derm MOA and Absorption
Inhibits cell division
Minimally absorbed normally, increases x10 with plastic wrap occlusion, also increases in inflamed skin/extensor surfaces
Downfall to Occluding Steroid Treatment?
Can increase potency which increases systemic side effects
Where/how long can you use Class 1 (super high potency) steroids?
Scalp, palms, soles, thick plaques in severe dermatoses for <3 weeks
Where/how long can you use class 2-5 (med-high potency) steroids?
Flexor surfaces for <6-8 weeks
When/how long should you use class 6/7 (low potency) steroids?
Large areas/thin skin-face, eyelids, genital and intertriginous areas
Can do 1-2 week intervals
Class 1 Topical Steroids
Clobetasol Propionate cream or ointment
Class 2 Topical Steroids
Betamethasone cream or ointment
Fluocinonide cream, gel, ointment or solution
Class 3 Topical Steroids
Betamethasone cream/lotion (0.05%), ointment (0.1%)
Triamcinolone acetonide ointment
Class 4 Topical Steroids
Fluocinolone acetonide ointment, triamcinolone acetonide cream or ointment
Class 5 Topical Steroids
Fluocinolone acetonide cream, desonide ointment
Class 6 Topical Steroids
Triamcinolone acetonide cream, desonide cream
Class 7 Topical Steroids
Hydrocortisone cream, lotion, ointment; available OTV
Systemic Side Effects of Topical Steroids
Cushing’s syndrome, pseudotumor cerebri, growth retardation, Na retention/edema, suppression of hypothalamic-pituitary-adrenal axis
Ocular Side Effects of Topical Steroids
Catarct, glaucoma, slowed corneal abrasion healing, extension of herpetic infection, increased susceptibility to bacterial or fungal infection
Cutaneous Side Effects of Topical Steroids
Atrophy, stretch marks, telangiectasis, purport, hypo pigmentation, slow wound healing, allergic dermatitis