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Pharmacy Year 2 Semester 2 > Kidney disease 2 > Flashcards

Kidney disease 2 Flashcards

1
Q

What is AKI?

A

“It is a clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes…”

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2
Q

AKI risk factors

A 
AGE >65
Clinical
Acutely unwell/ sepsis 
Hypovolemia 
(diarrhoea, vomiting, increased fluid loss or reduced intake
Hypotensive
Systolic Bp <100mmHg or more than 40mmHg less than baseline
Co-morbidities
Chronic kidney disease (CKD 3-5)
Heart failure
Diabetes mellitus
Liver disease
Atherosclerotic vascular disease
Nephrotoxic drugs 
ACE/ ARB, NSAIDs, Diuretics, Contrast
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3
Q

AKI common drug causes

A 
Inherent nephrotoxic potential
Dose
Duration of therapy
Frequency
Route of administration
Previous exposure
Drug interactions – additive effect if 2 nephrotoxic drugs are given together
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4
Q

How is AKI detected

A

Detection by any of the following:
A rise in serum creatinine of 26micromols/l or more within 48 hours
A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
A fall inurine output to less than 0.5ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
25% of greater fall in eGFR in children and young people within the past 7 days

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5
Q

AKI life threatening?

Clinical symptoms/signs

A

Can be life threatening – mortality in hospital ~50% if require dialysis
Frequently reversible and rapid recognition and treatment may preserve function
More common in older patients (esp 80-89 yr old) and those with CKD
Abrupt fall in glomerular filtration rate
Sustained rise in urea and creatinine
Potentially life threatening due to volume overload, hyperkalaemia and metabolic acidosis

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6
Q

Causes of AKI types and percentages

A 
Pre-renal = reduced renal perfusion =85%
Renal = 10%
Post-renal = obstruction = 5%
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7
Q

functions of kidney
specific
filtration
regulation

A

Filtration - removal of nitrogen-containing waste products

Regulation - acid/base, blood volume, haemoglobin, electrolytes

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8
Q

Pre-renal causes of AKI

A 
dehydration
sepsis
hypotension
shock 
hepatorenal syndrome 
severe heart failure
intra-abdominal hypertension/compartment syndrome
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9
Q

Renal causes of AKI

A 
NSAIDS
ACEi
ARBs
Gentamicin
GN/vasculitis (GN=glomerulonephritis) 
contrast 
interstitial nephritis 
myeloma
rhabdomyolosis
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10
Q

post-renal causes of AKI

A

prostrate enlargement
renal stones
pelvic cancer

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11
Q

Potential causes by drugs

A

SAD MAN

Sulphonylureas e.g. gliclazide 
ACE and ARB e.g. ramipril/losartan 
Diuretics e.g. furosemide 
Metformin 
Aldosterone antagonists e.g. spironolactone 
NSAID e.g. ibuprofen, naproxen
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12
Q

When to consider haemodialysis

A 
Fluid overload-resistant
High K (hyperkalaemia) > 6.5 with ECG changes or >7 mmol/l even with normal ECG-resistant
Pericardial rub
Uraemia/Encephalopathy
Metabolic acidosis-resistant
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13
Q

Common nephrotoxic drugs

A 
drugs of abuse - cocaine, herione etc 
statins - gemfibrozil  
antibiotics -aminoglycosides, ciprofloxacin, tetracycline, quinolones
Heavy metals
Chemotherapy
Immunosuppresants
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14
Q

Renal replacement therapy

A

Dialysis
Haemodialysis
Peritoneal dialysis

Transplantation
Live donor
Cadaveric
Non-heartbeating

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15
Q

Dialysis

A

Diffusion of molecules in solution across a semi permeable membrane along an electrochemical concentration gradient.

Haemodialysis
Synthetic membrane
Peritoneal dialysis
Endogenous (peritoneum)

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16
Q

Management of ESRF with haemodialysis
advantage of HD
disadvantages

A

advantages
-good removal of electrolytes

Disadvantages 
anaemia
hypotension
anaphylactic reaction to filter
air embolism 
access surgically introduced
cost
clotting and blocked lines
infections 
cramps
pain - chest and back
pruiritis
dysrhythmia
17
Q

How to deal with hypotension associated with dialysis and what is the cause

A

Cause: Too much fluid is being removed too quickly
Bolus of NaCl 0.9%
Omit blood pressure medicines
reduce rate of fluid removal

18
Q

how to deal with cramps associated with dialysis and what is the cause

A

Caused by hypotension and fluid removal

Give:
IV fluid
Quinine tablets
Re-assess weight

19
Q

Cause of chest and back pain associated with dialysis and how to treat

A

Complement activation
Inducement of angina

Treatment:
More biocompatible dialysiser
Paracetamol

20
Q

Advantages of PD (Peritoneal dialysis)

A
  • Fluid balance less tight

- renal function declines less rapidly

21
Q

Disadvantages of PD

Complications (long-term)

A 
Constipation
Infections
Pleural effusions
Scelorising peritonitis 
diabetes
electrolyte removal not as good as with HD

Long term complications: CVD, sepsis

22
Q

types of kidney transplant donor

A

cadaver

Living
Related
Matched unrelated

Non heart beating

23
Q

Immunosuppressive agents used in kidney transplant

A

Induction Therapy given in transplant centres at time of transplant
Maintenance therapy taken daily may include a combination of

Ciclosporin or tacrolimus +/- prednisolone
Ciclosporin or tacrolimus +/- prednisolone +/- mycophenolate or azathioprine
prednisolone +/- mycophenolate or azathioprine

Sirolimus

Aggressive treatment for rejection given in hospital methylprednisolone, ATG
Plasma exchange
Rituximab

24
Q

Ciclosporin
Tacrolimus
Sirolimus

Monitoring
Therapeutic changes
Cautions

A

Immunosuppressants

Require therapeutic drug monitoring as narrow therapeutic range
The therapeutic range changes over time since transplant
Caution with drug interactions
Caution with different brands (should be brand prescribing even for “generics”)

25
Q

Drugs that increase ciclosporin/tacrolimus levels

A
  • Amiodarone
  • Erythromycin
  • Clarithromycin
  • Ketoconazole
  • Fluconazole
  • Diltiazem
  • Nifedipine
  • Progestogens
26
Q

Drugs that decrease ciclosporin/tacrolimus levels

A 
Rifampicin
Carbamazipine
Phenytoin
Phenobarbitone
St John's Wort
27
Q

Management of common CKD complications

A

reduce gastric acidity with ranitidine or PPIs eg omeprazole

vitamin supplementation (Vit C, Vit Bs) caution with vitamin A accumulation

Quinine/ clonazepam for restless legs syndrome

Constipation due to fluid restriction

hyperlipidaemia: treating is controversial as currently less evidence than in general population

Antiplatelet therapy vs risk of bleeding

28
Q

Effect on bioavailability

A

GI absorption is decreased in patients with ureamia
GI symptoms are common eg nausea
small bowel absorptive function is decreased
first pass metabolism is altered
systemic concentration may be increased or decreased.

29
Q

Effects of kidneys on distribution

A

Apparent volume of distribution (Vd) of drugs is affected by renal insufficiency
oedema and ascities increase the Vd of highly water soluble drugs or protein bound drugs resulting in lower plasma concentrations
dehydration or muscle wasting may have the reverse effect
Altered protein binding can be seen

30
Q

Effect of kidneys on metabolism

A

Renal failure affects drug biotransformation: reduction & hydrolysis
normal rates of glucuronidation, sulphated conjegation and microsomal oxidation occur
many active or toxic drug metabolites depend on renal function for elimination, consequently pts with RF experience a high incidence of adverse drug reactions

31
Q

Renal excretion depends on?

What are some important factors to consider?

A

Depends on
glomerular filtration
renal tubular secretion
re-absorption.

Important factors to consider are water solubility, protein binding, molecular size, distribution.

32
Q

Patient adhere in CKD

A

Patients with CKD take on average 10 medicines per day – not automatically exempt from prescription charges
Long term condition = long term drug therapy
Experience increased incidence of side effects
May be managed by multiple health care providers eg – Specialists in hospital, GP, Practice Nurse

33
Q

Analgesics in kidney disease

Dos and don’ts

A

First choice - paracetamol,
consider reduced dose.
NSAIDs – ibuprofen, diclofenac both available OTC.
Avoid where possible, recommend short course only. Increased risk of adverse effects
Opiods
with caution – accumulation of metabolites
Use of topical preparations may carry less risk
capsaicin rub

34
Q

Opiods

A

Morphine
metabolised to morphine 6- glucuronide & morphine 3- glucuronide
M6G active metabolite excreted by kidneys therefore will accumulate in renal failure
half life increased to ~ 50 hours
Alternative choices – oxycodone, fentanyl, hydromorphone
Remember codeine is metabolised to morphine

35
Q

coughs and colds in patient’s with kidney disease

A

Patients with kidney disease are immunocompromised
Increased risk of infections
Symptomatic relief but early referral
Consider blood pressure effects of sympathomimetics – eg pseudoephedrine
Recommend simple measures eg, simple linctus, steam inhalations.

36
Q

alternative/complementary medicines

A

alternative therapy
Herbal medicines have been estimated to account for ~35% of acute renal failure in some African countries
Base compounds may be safe however some products contain traces of other chemicals which may cause harm

Pharmacy Year 2 Semester 2 (33 decks)

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