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Pharm 2 > Renal pharm > Flashcards

Renal pharm Flashcards

1
Q

what happens in the kidney

A
  1. Filter
  2. Reabsorb
  3. Secrete
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2
Q

How do we measure Kidney fxn?

A
  1. GFR- dependent on protein load
  2. Tubular secretion and reabsorption
  3. Endocrine and metabolic fxn
    -secretion of renin
    -produce and metab prostaglandins and kinins
    -EPO production
    -activate Vitamin D
    -Gluoneogensis
    -Metab of insulin, steroids, xenobiotics
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3
Q

Lab procedures to detect kidney disease?

A
  1. Urinalysis- pH, glucose, Ketones, nitrite, leukocyte esterase, heme, protein/albumin, specific gravity
  2. Microscopic analysis of urine- hematuria, WBC, CASTS, CRYSTAL (uric acid crystals)
  3. Serum or Blood Urea Nitrogen- urea undergoes filtration and reabsorption up to 50%
  4. Serum and Urine creatinine- most important endogenous biomarker for kidney disease = HIGH = DYSFXN
  5. Serum and urine Cystatin C= LOW= DYSFXN
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4
Q

Measurement of Kidney fxn

A
  1. Gold standard= mGFR= early rec of CKD and drug dose adjustment
  2. Conditions that impact kidney fxn independent of underlying pathol-> oral protein load (vegetarians have lower GFR) or Decline in kid mass- Age, HTN, or DM
  3. GFR is volume of plasma filtered across glomerulus per unit of time= based on total renal blood flow and cap hemodynamics (normal values= 120 mL/min/ 1.73 m2
  4. mGFR is equivalent to renal clearance of the solute marker- endog or exog
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5
Q

Caveats to reliability of Creatinine based Kidney fxn

A

ONLY USEFUL FOR STABLE RENAL FXN
CrCl= (urine Cr* Urine volume)/(plasma Cr* Time)

Not used when:
unstable= pregnancy, serious comorb, hospitalizes, EXTREMES IN MUSCLE MASS AND DIET

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6
Q

Formulas for dosing adjustments in CKD

A
  1. Cockcroft-Gault method = CrCL
    -direct measure of renal fxn
    - used to be the gold standard= phasing out
  2. Modification of diet in renal disease- MDRD= GFR
    -estimates GFFR based on creatinine and patient characteristics
    MAY UNDERESTIMATE ACTUAL GFR OF HEALTHY PT BY UP TO 29%
    BELOW 60 GFR
  3. CKD- EPI equation= GFR
    -near or ABOVE 60 ml/min
    -accounts for sex and race

CrCl= normal= 20 mg/kg/day
Nrml GFR= 100-120 mL/min

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7
Q

Chronic kidney disease

A
  1. ABN kidney structure or function for AT LEAST 3 MONTHS
  2. IRREVERSIBLE DAMAGE TO THE NEPHRONS
  3. Progressive decline of GFR over months to years
  4. Defined: Absolute GFR less than 60 or struct/functional abnormalities= hematuria, proteinuria, abn renal imagin

u/s: cysts, masses, renal artery stenosis-> Diag KD

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8
Q

How does CKD affect drug therapy

A
  1. pts more vulnerable to a drugs effect-> increases susceptibility
  2. Drug effect may be exaggerated or reduced
  3. may have higher steady state in renal disease-> toxicity results
    -ADME- absorption, distribution, metabolism, elimination

overall: Renal disease either increases of decreases drug effect-> usually increase= TOXICITY

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9
Q

Drug dose should be reduced proportionally to the predicted reduction in drug clearance

A
  • increased drug clearance= lower drug conc
    -Decreased drug clearance=higher drug conc and greater drug effect=====REDUCE DOSING OF THESE DRUGS
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10
Q

Pharmkinetics in CKD- Drug Absorption

A

Absorption
-alters abso or bioavial -> highly variable
Reasons= drug interactions
- GI-» DELAYED GASTRIC EMPTYING, DECREASED GASTRIC ACIDITY, INCREASE IN GASTRIC PH

high use of antacids-> increases pH= cdkd pts freuently take

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11
Q

Pharmkinetics in CKD- Drug Distribution

A

Volume of distribution INCREASED-> DECREASING SERUM DRUG CONC
due to
-fluid overload secondary to fluid intake or administration
-decreased protein binding-> increased tissue binding

Altered plasma protein binding
-normal kidney fxn->protein binding limits drug distribution as only unbound are able to cross cellular membranes and distribute

CKD= decrease in binding= increased drug distribution

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12
Q

Example of drug distribution

A

Protein binding of phenytoin (90% protein bound-> primary to albumin) (decreased binding= not activated-> into tissues)
-decreased due to decreased plasma phenytoin binding affinity for albumin
-changes alter relationship btwn total phytoin conc and desired/toxic effects
-resulting increase in unbound fraction from values of 10% in normal to over 20% in G5 CKD= increased hepatic clearance and decreased total conc

IN CKD THERAPEUTIC RANGE BASED ON TOTAL PHENYTOIN CONC IS SHIFTED DOWNWARD FROM NORMAL VALUES OF 10-20 TO 4-8

Drawing drug level decreases bc unattached= only looking for active which has to be bound

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13
Q

Pharmkin in CKD: Elimation

A

Kidney fxn is most quantifiable determinant of drug clearance-> how quickly a drug is removed from the body

fxn is combined process of
-GFR
-tubular secretion
-reabsorption
-reduced kidney mass
-# of functioning nephrons
-Renal blood flow

alteration of fxn can have dramatic effect on drug disposition-> drugs primarily filtured thru kidneys a decrease in GFR= PROPORTIONAL DECREASE IN RENAL DRUG CLEARANCE

clearance decreased in both renally and non renally

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14
Q

Pharmcodynamics

A

pharmacodynamics= effects of drugs and the MOA on body

Decreased GFR= slows rate of drug filtration thru kidney and decreased clearance
-increased conc levels in blood= diff peak and trough serum conc

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15
Q

Causes of CKD requiring dose adjustments

A
  1. Age decreases fxn
  2. Multiple medical comorb= 1. DM 2. HTN
  3. Medications alter kidney fxn= 1.NSAIDS 2. Metformin
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16
Q

Drug dosing in CKD

A
  1. inapprop dosing can cause -> toxicity and ineffective therapy
  2. Special concerns in elderly-> Age related decline in GFR or polypharmacy
  3. Active/toxic metabolites
17
Q

Renal metabolism

A

some drugs undergo partial renal metab-> affect adjustment
loading dose and maintenance dose
Volume distribution= increase water= increase VD so increase dose and vice versa

18
Q

Drug dosing regimens for CKD pts

A
  1. loading dose is the same as pts with normal= no adjustments
    -except if VD is known to be altered in presence of CKD or concomitant disease
  2. Rapid achievement of therapeutic drug conc is important= start aggressively like in anticoag, sepsis, stroke pts
  3. FDA product labeling should be foundation for ongoing therapy
19
Q

Renal dosage adjustment

A
  1. if pts renal fxn is markedly decreased -> drugs will need renal adjustment but varies
  2. online calc available for CrCl
  3. no simple method applies to all drugs
  4. Dose reduction vs longer interval
    -50 mg x2 = more steady state but wont excrete fully = toxic effect
    -100 mg x1= peak and trough but excrete so less toxic
20
Q

Important drug considerations in CKD

A
  1. antibiotics
  2. Antihypertensives
  3. Antidiabetic agents
  4. Analgesic agents
21
Q

Antimicrobial agents in CKD that need dosing adjustment

A
  1. Penicillin G or carbenicillin
    -neuromusc toxicity, myoclonus, seizures, coma
  2. Tetracyclines (NOT DOXY) exacerbate uremia
  3. Nitrofurantoin metabolites cause peripheral neuropathy
  4. AMINOGLYC SHOULD NOT BE USED IF POSSIBLE= NEPHROTOXIC
22
Q

Problems with Fluoroquinolones

A

Cipro/Levaquin
Moxifloxacin - no renal adjustment
—all increase QT intervals—
1.Loading doses are okay
2. Renal dosing is 1/2 to 1/4 “normal dose”

23
Q

antihypertensive agents- drug considerations diur

A

Diuretics
-THIAZIDE DIURETICS NOT RECOMMENDED IF SERUM CREATININE GREATER THAN 2.5 MG/DL OR CREATININE CLEARANCE LESS THAN 30 ML/MIN
–loop diuretics mc for uncomp htn in ckd
–potassium sparing diur and Aldosterone blockers= increase SERUM POTASSIUM which wont get excreted

24
Q

Anti HTN agents- ACE and ARBS

A

ACE and ARBS
-1st line for pts with DM and Early Kidney Disease

problems
-ACE ADN ARBS DECREASE GFR AND INCREASE CREATININE

DC IF SERUM CREATININE INCREASES MORE THAN 30% OR SERUM POTASSIUM AT LEAST 5.6

25
Q

Anti HTN- renal adjustment

A

Adjustment:
Hydrophilic BB= ATENOLOL AND NADOLOL

No adjustment: not hydrophylic
CCB, CLONIDINE, ALPHA BLOCKERS

Water loving go to increased water conc-> impaired excretion= increased build up of drug

26
Q

Metabolic agents- Metformin

A

BBW: LACTIC ACIDOSIS W/ CERTAIN COMORB-> blocks gluconeogenesis= increases lactic acid

Do not give met if :
1. SERUM CREATININE IS GREATER THAN 1.5 MG IN MEN OR 1.4 IN WOMEN
2. Age over 80
3. CHF

dont avoid-> start low dose and titrate with close monitoring

Temp d/c metformin in pts at higher risk of lactic acidosis-> Sepsis or AKI

SE: diarrhea

27
Q

Metabolic agent- other

A
  1. Sulfonylureas- (Glimepiride or glyburide)
    -CAUSE HYPOGLYCEMIA NOT USED IN STAGE 3 OR HIGHER KIDNEY DISEASE
    -no adjustment of GLIPIZIDE
  2. Statins
    -adjustment for all but ATORVASTATIN
28
Q

Mnemonic for bad

A

TVBMANSIAACKFP
These-tetracycline, thiazides
Very- vancomycin
Bad- BB
Meds- metformin
Are- ACE/ARB
Not- Nitrofurantoin/nsaids
Safe-Sulfonureas
In- Imepenem
Acute- Aminoglycosides
And- Acyclovir
Chronic- Chemo drugs
Kidney- K+ sparing diuretics
Failure- Fluoroquinolones
Patients- penicillins

29
Q

Insulin and CKD

A
  • Hormone synth and secreted by pancreatic islet cells
  • Decreased GFR = increased insulin levels-> kidney clears 30-80% of serum insulin
    -Dose may need to be reduced to avoid hypoglycemia
    -Done empirically as pts are doing daily monitoring of BF
30
Q

Analgesic agents and CKD

A
  1. Opiods
  2. NSAIDS

acetaminophen- no adjustment needed

31
Q

Opioid use and CKD

A

AVOID MORPHINE AND CODEINE

MEPERIDINE AND TRAMADOL METABOLITES-> affect central nervous and respiratory systems= not recommended in stage 4 or 5
-hydro morphine, oxycodone, and fentanyl are safe

Renal toxicity appears in appropriate use-> higher than needed doses, presence of other toxins, pre-existing dehydration, PROSTATE ENLARGMENT= DECREASED URINE OUTPUT LEADING OT KIDNEY FAILURE

Chronic opioid use= greater incidence of toxicity
- accumulate metabolites - cause unwanted side effects-> steady state reached and builds up

32
Q

Opioid use/ overdose

A

Overdose= AKI
causes: dehydration, hypotension, rhabdomyolysis, urinary retention

CKD may result due to mode of administration of drug
-skin popping resulting in amyloidosis
-Heroin associated nephropathy (HAN)

33
Q

Opioid and elderly

A

age related changes might alter opioid drug kinetics= unwanted SE
-Decreased organ fxn of liver and kidney
-Alterations in ADIPOSE TISSUE COMPOSITION ALTERING KINETICS- allow metab to accumulate and present for longer

34
Q

Nonsteroidal anti-inflammatory drugs NSAIDS

A

Indications: Chronic inflammatory conditions, Acute and Crhonic pain, Fever
-Aspirin
-indomethacin
-Diclofenac
-ketorolac
-ibuprofen
-naproxen
-celecoxib

SE: Gastrointestinal complications, NEPHROTOXICITY, Nervous sys effects-> sodium retention, hyperkalemia, type 4 RTA, hyponatremia, AKI

—constricts afferent arteriole and decreases GFR—

35
Q

NSAIDS: Renal Syndromes

A

AKI
Metabolic disturbances-> doesnt filter= hyponatremia, hyperkalemia, metabolic acidosis
Acute and Crhonic interstitial nephritis
decreased sodium excretion -> peripheral edema, htn, exacerbated hf
HTN-> develops or exacerbated by use

36
Q

NSAIDS: AKI

A

linked to 3x higher risk for acute renal failure-> due to reduced renal plasma flow bc of decreased prostaglandins which reg VD at glomerular level

Adjustment if agent specific

RF make kidney dependent on prostaglandins:
1. “True” intravasc Volume depletion-> vomiting, diarrhea
2. “Effective” intravasc volume depletion-> CHF, cirrhosis, nephrotic syndrome
3. Kidney disease: acute or chronic
4.Meds: ACE and ARBS
5. Old age

37
Q

NSAIDS and CKD

A

cause or worse? unknown
SHOULD BE AVOIDED IN PTS WITH STAGE 4 OR 5 CKD

38
Q

NSAIDS overall

A

Antihypertensive effects of BB, ACE or ARBs= can be decreased
Short term use is well tolerated if
-well hydrated
CrCl>50%
no HF, DM, HTN
no long term use recommended
Serum creatinine should be checked every 2-4 weeks in early tx

Pharm 2 (15 decks)

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