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Pharmacy Yr3 Renal and hepatic diseases > Week 2- Assessment of renal function & drug handling in renal disease+ classification > Flashcards

Week 2- Assessment of renal function & drug handling in renal disease+ classification Flashcards

1
Q

what is the main function of the kidney?

A
  • its an Excretory organ

- but also has a metabolic and endocrine function

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2
Q

what can occur if there is a failure in the excretory function of the kidney?

A

accumulation of drugs + toxicity in renal failure

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3
Q

what needs to happen if the patient has renal failure?

A

– assess degree of renal impairment
– make adjustments
– change to safer drug
– avoid nephrotoxics

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4
Q

what tests are done to asses renal function? tests on the plasma?

A

– Creatinine
– Urea
– eGFR

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5
Q

what tests are done to asses renal function? tests on the urine?

A 
– Albumin:creatinine
ratio (ACR)
– Osmolality
– Specific gravity
– Proteinuria/
Microalbuminuria
– Haematuria
– Mid stream urine
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6
Q

what is creatinine?

A

• By product of protein metabolism, freely filtered by the kidneys

  • if there is a kidney problem creatinine levels will rise as its not being cleared
  • GFR ≈ Cr Cl
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7
Q

what is the best way to measure creatinine clearance?

A

-24hrs urine collection
Cr Cl [ml/min] = Urine Cr [mol/l] x Volume [ml] /
plasma Cr [mol/l] x Time

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8
Q

what are some limitations of urine collection for creatinine clearance?

A
  • Accuracy of urine collection (might forget by patient)

* Time delay in getting results by to the lab

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9
Q

what other method is done to calculate creatinine clearance? equation = cg

A

Cockcroft & Gault Equation:

Cr Cl [ml/min] =
[140-age] x IBW x F /
Plasma Cr [mol/l]

[F = 1.23 males & 1.04 females]

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10
Q

what are the limitations for Cockcroft & Gault Equation?

A

– Assumes average population data
– Unsuitable for children (separate calculation) &
pregnancy
– Renal function must be stablely off

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11
Q

what is the normal creatinine clearance?

A

Traditionally, assuming “normal” CrCl = 120ml/min

and “normal” Cr = 55-125 µmol/l

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12
Q

what is another way to calculate renal impairment?

A

eGFR THROUGH BLOOD SAMPLE

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13
Q

what 4 variables are used to calculate eGFR?

A

serum Cr, age, sex, ethnic origin

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14
Q

what are some limitations of eGFR?

A

(children, ARF, pregnancy, oedema etc)

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15
Q

how many stages is there for renal impairment when using eGFR?

A

5

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16
Q

what are the different stages of renal impairment for eGFR?

A
  • Stage 1 (G1) >90 Normal GFR
  • Stage 2 (G2) 60-89 Mild impairment
  • Stage 3A (G3a) 45-59
  • Stage 3B (G3b) 30-44 Moderate impairment
  • Stage 4 (G4) 15-29 Severe impairment
  • Stage 5 (G5) <15 Established/End stage
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17
Q

how do you improve accuracy and find out someone’s absolute GFR ? equation

A

GFR absolute =
eGFR x individual BSA /
1.73

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18
Q

what other blood test is used to work out an individual renal impairment?

A

urea

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19
Q

what is urea?

A

• Breakdown product of protein metabolism
-if patient has impairment levels will rise in the blood
• > 15mmol/ l = uraemia (Ref: 1.7-6.7 mmol/l)

20
Q

when would you also have raised levels of urea other than in renal impairment?

A
  • increase levels also occur in:
  • dehydration
  • excess protein intake
  • haemorrhage
  • severe infection
  • muscle injury
  • catabolism
21
Q

what are the 3 blood tests for renal impairment?

A
  • urea
  • creatinine
  • eGFR
22
Q

what can be found in urine showing development of renal impairment

A

albumin

23
Q

what are he levels for albumin:creatinine ratio that shows possible risk of renal problems?

A

– >70mg/mmol in non-diabetics
– >2.5mg/mmol (males) & >3.5 (females) diabetics
– ► Increased risk of developing renal disease

24
Q

what are some other urine tests for renal probelms?

A

– Osmolality
– Specific gravity
– Haematuria
– Mid stream urine

25
Q

what kind of symptoms can high levels of urea in the blood give ?

A

-vomiting, diarrhoea, g.i.

oedema

26
Q

how is absorption affect due to renal problems?

A

• Uraemia  vomiting, diarrhoea, g.i.
oedema which affects and reduces the absorption of oral drugs
• decrease calcium absorption
• Phosphate binders

27
Q

how is distribution affect due to renal problems?

A
  • changes in hydration due to fluid accumulation which could affect water soluble drugs
  • uraemia as it competes with drugs for binding sites like protein and tissue, due to competition would have raised level of drugs and risk of toxicity tissue binding e.g. digoxin, protein binding e.g. phenytoin
28
Q

how is metabolism affected due to renalporblems?

A 
• decrease activation of Vitamin D
• decrease insulin metabolism
• decrease elimination of pharmacologically active
metabolites:
– Eg:
• nor-pethidine
• morphine 6-glucuronide
29
Q

how is excretion affected by to renal problems?

A
  • Most important factor

* Dose modification maybe necessary

30
Q

when talking about dose adjustments what is included?

A 
• Achieved by:
– decrease dose
– increase dosing interval
– Combination of both
• LOADING DOSES: no adjustment
31
Q

what is the function of the kidney?

A
  • Regulatory, water and electrolytes
  • Excretory- toxins, fluid,
  • Endocrine, angiotensin vitamin D
32
Q

how do you classify renal disease?

A

cause

reversibility

33
Q

how do you classify renal disease through cause?

A

• Pre-renal failure:
• Intrinsic renal failure
-Post-renal failure

34
Q

what is pre-renal failure

A 
-before the renal damage
• Pre-renal failure:
– ↓ renal perfusion:
– Egs:
• Hypovolaemia (burns, dehydration,
haemorrhage)
• Infection
• Liver disease
35
Q

what is Intrinsic renal failure? examples

A 
– Damage to renal tissue:
– Egs:
• Glomerular (e.g. diabetic nephropathy,
glomerulnephritis)
• Tubular (e.g. interstitial nephritis)
• Renovascular (e.g. HT)
• Infection
• Nephrotoxicity
• Metabolic (e.g. hypercalcaemia,
hyperuricaemia)
• Congenital (born with it)
36
Q

what is Post-renal failure?

A

– Obstruction to urinary flow
– Egs:
-back pressure in the kidney and cause scarring
• Stones (eg calcium oxalate)
• Structural (eg tumour, stricture, prostatis)
• Nephrotoxicity
• Outside urinary tract (eg ovarian tumour)

37
Q

what are the different types for classification for reversibility of renal problems?

A 
-Acute kidney injury (acute renal failure)
• Chronic kidney disease (chronic renal
failure)
• End stage renal failure
• [Acute on Chronic renal failure]
38
Q

what is Acute kidney injury (AKI)? incidences

A

• Regulatory & excretory failure
• Usually secondary to decrease circulation
(pre-renal failure)
• Develops rapidly (hours/days), high
mortality (up to 90% if untreated –
multiple organ failure), but essentially
reversible
• 400-600 pts/million population/yr AKI
• Up to 200 pts/million population/yr AKI require dialysis
• 1 in 5 people admitted to hospital as emergency has AKI

39
Q

what is AKI defined as?

A

• ↑ Cr ≥ 26µmol/L within 48hrs
• ≥ ↑50% Cr from baseline, known or presumed to have
occurred in last 7 days
• ↓ urine output to <0.5ml/kg/hr for >6hrs

▪ Alert system in hospital blood test reports

40
Q

WHAT ARE SOME OF THE RISK FACTORS FOR AKI?

A
  • Previous AKI
  • Pre-existing CRF
  • Age >65yrs
  • CCF (CONGESTED HERT FARLURE)
  • PVD (VASULAR DISEASE)
  • Diabetes
  • Hepatic disease
41
Q

what are some trigger factors for AKI?

A
  • Sepsis or infections
  • Hypovolaemia (dehydration, bleeding)
  • Hypotension
  • Drugs: E.g. NSAIDs, ACEIs, ARBs, Diuretics
42
Q

how to prevent AKI?

A

• Avoid use of nephrotoxic drugs in those at risk
(e.g. avoid use of NSAIDs in elderly)
• Monitor renal function for drugs known to
cause renal impairment
• Review medication known to exacerbate AKI
(e.g. temporarily withhold ACEIs, diuretics etc
if patients become acutely unwell – “Sick
rules”)

43
Q

WHAT ARE THE SIGNS AND SYMTOMS OF AKI?

A 
• Volume depletion:
– Thirst
– Fluid loss ++
– Oliguria
– Dry mucosae
– DECREASE skin elasticity
– Tachycardia
– Hypotension
– DECREASE JVP
• Volume overload (if left
untreated):
– INCREASE orthopnoea / paroxysmal
nocturnal dyspnoea (PND)
– SOA swelling of ankles
– Oedema
– Pulmonary oedema
– Pulmonary crackles
44
Q

what s the treatment for AKI?

A 
• Aim to eliminate cause, restore &
maintain RF
– Restoration of renal perfusion:
• IV fluids (eg Sodium chloride 0.9%)
• Blood
– Dialysis if needed to maintain function whilst
underlying cause is managed
– Review drug therapy – stop/withhold
nephrotoxic drugs
Loop diuretics
• E.g. Furosemide, (bumetanide)
• Produces diuresis, reduce tubular cell
metabolic demands & increase renal blood
flow (increase renal PG)
• Caution to avoid further dehydration
• Doses up to 1-2g iv over 24 hrs
• Maximum rate 4mg/min ( higher rates
cause ototoxicity)

Dopamine
• Low dose (2 mcg/kg/min)  renal
vasodilatation mediated through DA1
receptors
• leading to increase renal perfusion & urine output
• [Higher doses (>5 mcg/kg/min) → vasoconstriction therefore care
with dosing]

other:
• Antibiotics:
– If infective cause
• Correction of electrolyte abnormalities
e.g. hyperkalaemia (see later)
45
Q

what is Chronic kidney disease? incidences?

A

• Regulatory, excretory & endocrine failure
• Usually secondary to renal tissue
damage
• Insidious & slow onset
• High degree of renal reserve leadsto usually
irreversible by time patient presents with
symptoms
• ~ 4% > 18yrs CKD Stages 3-5 (30-45% in >75yrs)
• 1.5 x in men than women
• 3-5 x in Afro-Caribbean & Asian

46
Q

what is end stage renal failure? incidences

A

• Eventual progression from CKD
• Renal replacement therapy needed
[i.e. dialysis or transplantation]
• 110-120 new cases/million population/yr

47
Q

what is acute on chronic renal failure?

A 
• Patient’s with pre-existing chronic
renal impairment
• Sudden rapid decline in renal function
due to an underlying cause e.g.
dehydration, infection, drugs

Pharmacy Yr3 Renal and hepatic diseases (5 decks)

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