Wk 5 Flashcards
(276 cards)
What are changes of the kidney w aging
Glom changes…. Sclerosis obsolescence (can vanish)
Interstitial fibrosis
Tubular atrophy secondary to reduced tubular volume and length.
Thickening of basement membranes
Arteriolar hyaline sis, fibro elastic hyperplasia.
Too much red!
Grossly:
Cortical thinning, smaller kidney size
Changes in fcn of kidney w age
Dec renal blood flow, grr, tubular NA reabsorption, K excretion (ie because less Na getting to distal tubule, also bc in part due to low renin and aldosterone levels)…. Edema, HTN,
Urineary concentration and dilution.
Kidney status dictated by
Urine sedimentation. Urinalysis w urine protein and casts etc. eGFR and serum Cr (not just function, which is via eGFR and Cr)
New eGFR categories? For chronic kidney dz
New albumin categories?
G1, G2, G3a and G3b, G4, G5
It is important to remember is pt in steady state or not… GFR is applicable to CKD.
A1-A3.. Low grade to high grade.
Use CKD epi formula
What are the main causes of CKD in the elderly ? 10% of population, most is mild or mod,
Primarily HTN +/- ischemic nephrosclerosis
- diabetic nephropathy, cardio renal syndrome
- renal vasculitis syndromes also more common.
Mgmt of CKD in elderly
Treat BP, DM, underlying conditions…. Don’t necesaRily want to be aggressive though. Bc ortho hypotn risk. Hypoglycemia risk, renal artery stenosis.
Minimize risk for AKI… Harm reduction
- w/d or with holding aceis and arbs.
Avoid NSAIDS
Avoid ECFV depletion (present early if volume depleting illness!
Serial lab monitoring: serum Cr, eGFR, electrolytes, Hgb, minerals, PTH, U/A, urine ACR.
adjust really eliminate medications. Risk of metformin due to lactic acidosis…. Don’t give if
Insults on kidney?
Dec pressure on outgoing side by blocking angio tension 2 At efferent.
Prostaglandin inhibitor ie NSAID or cox2 inhib reduces renal blood flow and GFR
DiureticS And dec volume status…
Triple whammy to kidney
NSAIDS effect on kidney
Sodium retention and htn
AKI, hemodynamically mediated.
- Ranges from reversible to necrosis
Acute or chronic interstitial nephritis (analgesic nephropathy)
Concentration in papilla… Die, slow, painful gross hematuria. Papillary necrosis.
Glomerulonephritis
Hyperkalemia
What are reversible factors
Acute illness, CHF, I’m, pna, ce
Lolita’s, gout flare, gastroenteritis, food poisoning
Vol- dep,eating diuretics
Meds: NSAIDS, ace ARB, aminoglycosides, uv contrast dye, Otis.
Obstruction- abdo ultrasound indicated if
What is mortality in hospital if dialysis started?
RRT up to 50% in hospital, not ,ugh diff in younger ppl.
What are components of high morbidity in dialysis?
Hypotension, falls, access, infections.
Candidacy probably best based on baseline fcn status / comorbid it’s burden.
Gfr declines with as due to
Neohrosclerosis
When to stop the ACEi when it becomes effective and changes to detrimental
No set value, depends on clinical picture. Some benefit up to gfr of 15
What does it mean for a drug like phenytoin to be a zero order drug?
Zero order drug means half life changes with dose and will be about 85% of steady state at 7 days. Draw within first couple days to get an idea of if you are in therapeutic window. set amount cleared over time independent of amount in body. Therefore half life is always changing depending on how much drug is in there. So if you give high amounts that saturTe tissues, then small dosage apchange wpcan sky rocket.
Vs 1st order…. Eliminated based on fraction (ie percentage per unit time) in body. This is how we get half life…. Think usually 5-6 half lives will eliminate from body.
Why must phenytoin be given at 50 mg/min max?
Risk of faster infusion is hypotension and cardiovascular collapse because of propylene glycol.
Why does albumin level matter with phenytoin?
Phenytoin is hig,y protein bound, as are most meds.
Usually is 90% bound to proteins so 10% is free and active.
If low albumin ie 44, then not enough binding. Total concentration is same (think its happy because in range), but if albumin super low then may actually be toxic and therefore must correct for amount of free drug.
What is the difference between high dosing extended interval HDEI vs traditional?
Aminoglycosides are concentration-dependent killing drugs. So giving more bang for buck. (As is Fluoroquinolones… Therefore can dose adjust to 500 once a day instead of 250 bid)
Vs traditional which is less at higher freq.
With huge peak, killing more
Also post-antibiotic effect … High conc penetrates inside cell and this can’t measure in plasma but is still acting while giving …. So eliminates quickly because 1st order kinetics…. Therefore by 18 renal has cleared out and now toxicity- free period for organs to rest while ears and kidney relax.
Saturable uptake…. Constant bathing of cells in gentamycin. Vs high peak which eliminates and gives free period w no bathing kidneys and ear.
Why is CKD a contra to gentamyinc HDEI? Ie exclusion Criteria
Bc doesn’t eliminate fast enough and builds to way higher levels over time.
Therefore majority of time don’t give to elderly bc inherent true fcn of kidneys not as good (even if Cr looks pretty good, half life is still going to be higher.)
(>75 yo)
Always want to have measurable trough level so organ is always bathed in antibiotic,.
Abn body comp ie burns, morbid obesity.
Neutropenia, meningitis. Endocarditis etc.
Ascite cf, cirrhosis,
Surgical prophylaxis…. Use conventional dosing.
When used for synergy ie endocarditis.
Should you do a post level for aminoglycosides?
No, just do pre-level if you are to measure anything. Should be 0 in blood for 18-24 hours but dont actually need to measure this. Bc if you think they are accumulating then just switch to traditional. If higher, then swap to traditional dosing. If you think renal function is suspect, just switch to traditional dosing
What is aminoglycoside dosed based on?
Lean of ideal body weight…. Extra body weight metabolizes drug differently.
This is aminoglycosides- specific.
Must compare IBW w actual BW.
Need to use dosing body weight (IBW + (0.4 x (adjusted body wt - IBW)
Multiply DBW x dose (6 mg per kg)
Round to administerable dose.
Conventional ordering of aminoglycosides
Pre and post 3rd.
When > 5 days
Elderly, 65-74 yrs.
Don’t need to orde routine serum peak and trough concentrations in HDEI
What to monitor patient for?
Vertigo, tinnitus, pressure fullness in ear, diplopia, pain, new onset hearing loss. Esp if > 5-7 days. Ie 4 wks for osteomyelitis.
Therapeutic drug monitoring and keeping in target range can still cause oto/vestibular toxicity.
What are constipation get meds?
Opioid (senekot is first line, this is a stimulant so reversing opioid action) anticholinergics, ondansetron, iron.
Osmotics : use PEG 3350
Rwctal tx: docolax
Also can use: peripheral mu receptor antagonists…. Methylnaltrexone. Don’t use if obstructed, is expensive,
How to treat n and v?
Target the pathophys that feed to the integrative vomiting centre.
- Drugs (chemo, opioids, dig), biochemical ie uremia, electrolytes, hyperCa, toxic (radiation, emetogenic peptides)
- GI tract vagal - distension… Over eating gastric stasis, mass, obstruction, constipation, chemical irritants (blood, drugs)
- Cerebral- high CNS..l.msensory,
- CHECK OUT SLIDES!!!!