Prescribing in Renal Dysfunction Flashcards
Which drug can be used instead of codeine which causes less constipation and should be considered in those with renal impairment?
Dihydrocodeine
Fentanly - used if codeine is not tolerated or ineffective
How is acute kidney injury classified?
Pre- renal
Renal
Post renal
What are the pre-renal causes of an AKI?
Associated with fallen renal blood volume which leads to falling GFR-
Hypovolaemia of any cause
- Dehydration
- Haemorrhage
- Nil by mouth
- Burns
- excessive Sweating
Hypotension without hypovolaemia
- Cirrhosis
- Septic shock
Low cardiac output/ cardic failure
- Cardiac failure
- Cardiogenic shock
- Arrhythmias
- Tamponade
- Cardiomyopathy
Renal loses
- Diuretics
- hyperglycaemia (osmotic diuresis)
Gut Losses
- vomiting
- nasogastric tube losses
- diarrhoea
Third space loses
- pancreatitis
- peritonitis
- bowel obstruction
What are the post renal causes of an AKI?
Obstruction of the urinary tract
- Bladder outflow obstruction (BPH in men)
- Bilateral ureteric obstruction - (stones and tumours in renal pelvis, ureter or bladder) Emboli
- Intraabdominal/ pelvic tumours compressing ureter
- Ureteric stricture (Tb, calculus, surgery)
- Infection (UTI, inflammation causing obstruction) causes hydronephrosis (swelling of kidney) and renal damage over time
What are the Intra - renal causes of an AKI?
Acute tubular necrosis (80-90%)
Disease affecting the intrarenal arteries and arterioles, as well as glomerular capillaries, such as - vasculitis - accelerated hypertension, - cholesterol embolism, - haemolytic uraemic syndrome, - thrombotic thrombocytopenic purpura (TTP), - pre-eclampsia and - crescentic glomerulonephritis
- Acute tubulointerstitial nephritis (can be caused by acute obstruction by crystals)
- Acute bilateral suppurative pyelonephritis
- Pyelonephritis of a single kidney, which can cause acute uraemia
What are some common causes of acute tubular necrosis?
- Renal ischaemia or direct renal toxins - drugs
- Haemmrrhoage
- Burns
- Diarrhoea and vomitting
- Pancreatitis
- Diuretics
- MI
- Congestive heart failure
- Endotoxic shock
- Hepatorenal syndrome
- Contrast neropathy (contrast given for images)
- Drugs
- Pre-eclampsia
Which drugs are toxic to the kidneys and can cause AKI’s? What effect can they have on the kidneys?
- Aminoglycosides (tubular necrosis)
- NSAIDS/cox 2 inhibitors -prostaglandins required for renal blood flow, Drug causes renal hypoperfusion and AKI
- ACE inhibitors
- Gentamicin
- Amphotericin B
- Cytotoxic chemotherapy
- Diuretics (volume depletion) (esp. spironolactone)
- Immunosuppressants ciclosporin and tacrolimus (renal vasoconstriction leading to ischemia)
- Lithium salts - Tubulo interstitial damage and Chronic kidney disease.
- Radiocontrast media- vasoconstriction and ischemia
- Cocaine
- insecticides, herbicides
Describes stage 1 of AKI
Stage 1-
Creatinine rise of 26 micromol/litre or more within 48 hours; or
Creatinine rise of ≥ x 1.5 from baseline in 7 days ; or
Reduced urine output of < 0.5 ml/kg/hour for more than 6 hours.
Describes stage 2 of AKI
Creatinine rise of ≥ x 2 from baseline in 7 days ; or
Reduced urine output of < 0.5 ml/kg/hour for 12 hours or more.
Lithium salts are nephrotoxic. How are they managed when it causes an AKI?
can cause tubulo-interstitial damage and chronic kidney disease with long-term use. However, it should only be suspended if there is known lithium overdose or toxic levels, due to its importance as a treatment for bipolar disorder. If the situation is unclear, discuss its use with a specialist.
Which pathological states are nephrotoxic?
Hypoperfusion
Sepsis
Rhabdomyolysis
Hepatorenal syndrome
How does sepsis cause an AKI?
endotoxins and inflammatory mediators from infection can damage the renal vascular endothelium resulting in thrombosis
How does Rhabdomyolysis cause an AKI?
myoglobin released from damaged muscles precipitates in renal tubules and also reduces blood flow in the outer medulla.
How does Hepatorenal syndrome cause an AKI?
patients with end-stage liver disease often have renal vasoconstriction.
Which equations are used to establish the estimated glomerular filtration rate (eGFR) and the Creatinine clearance?
Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula and normalised to a body surface area of 1.73 m2.
The Cockcroft-Gault formula - creatinine clearance
In most cases the eGFR is used as an estimate of GFR to determine renal function and drug doses. Under which circumstances is the Creatinine clearance recommended?
Older adults
Patients on a toxic medicine
Patients at extremes of muscle mass
Patients on a medicine with a narrow therapeutic index
Patients on direct-acting oral anticoagulants (DOACs)
In most cases the eGFR is used as an estimate of GFR to determine renal function and drug doses. Under which circumstances is the Creatinine clearance recommended?
Older adults
Patients on a toxic medicine
Patients at extremes of muscle mass (catabolic state, obese, under weight)
Patients on a medicine with a narrow therapeutic index
Patients on direct-acting oral anticoagulants (DOACs)
Children
Pregnancy
patients with reduced muscle mass (such as extreme old age, malnutrition, amputation, and other muscle disorders).
eGFR is not an accurate function of AKI it is better suited for CKD
List all the stages of drug kinetics and how they are effected by kidney dysfucntion
ADME
Absorption - most drug absorption is unaffected by reduced renal function.
Distribution - protein binding of some drugs are affected in renal impairment.
Metabolism - some hepatic processes are affected by renal impairment but only at severe levels.
Elimination - water soluble drugs are particularly affected.
How do the kidneys effect the half life of the drug?
he half-life will be prolonged in renal impairment if the drug (or active metabolites) is significantly removed by the kidney.
How can drug doses be adjusted in renal impairment?
Reducing the amount of the regular dose given, or
Extending the interval between regular doses (better for maintaining specific peak and trough concentrations).
How can the heart rate be used to identify hypovolaemia?
A rise in heart rate on standing of more than or equal to 30 beats per minute is one of the more sensitive indicators of hypovolaemia
Which parameters (bed side tests) and clinical observations should you assess when assessing fluid balance in AKI?
Pulse - supine and upright (where possible). You may need to sit the patient up in bed if they are unable to stand.
Blood pressure - supine and upright.
Arterial oxygen saturation.
Pulmonary oedema - examine for tachypnoea, fine bilateral basal inspiratory crackles, chest X-ray signs.
Fluid overload - check for pitting ankle and sacral oedema. Check the patient’s weight daily (rising daily weights are a very useful indicator of fluid overload).
What is used to replenish and maintain volume in AKI?
repeated fluid ‘challenges’ with infusion of 250 to 500 ml or more of sodium chloride 0.9% - Re-assess after every infusion
Monitor vital signs, including urine output, in an acute or high dependency environment.
Then -
Reduce the rate of infusion, more so if the patient remains oliguric.
Iatrogenic fluid overload risks pulmonary oedema and has recently been associated with increased mortality in AKI.
Reflex’ prescribing of up to 3 to 4 litres of intravenous fluids per day without proper fluid balance assessment is wrong and risks disaster!
If a patient has AKI with hypovolaemia and a metabolic acidosis, what would you use to replenish volume?
serum bicarbonate of less than 20 mmol/litre
What type of drug is Mefenamic acid?
NSAID
What effect would a calcium channel blocker have in someone with renal failure?
Causes hypotension which can reduce perfusion and make AKI worse
Which antimicrobials can be used to treat Pseudomonas aeruginosa?
Amikacin
Carbapenem
Which anatomical aspects of the urinary system need to be obstructed before symptoms of post renal AKI presents
Post renal AKI usually presents when the ureters in both kidneys are obstructed or the urethra is obstructed.
In post renal AKI and pre-renal AKI what are the clinical features which will present?
- GFR is decreased
- More urea and creatinine in the blood
(Azotemia- high levels of nitrogen containing waste compounds in the blood) - Oligurea- low levels of urine
- Reabsorbtion of urea is higher than that of creatinine so- BUN (blood urea nitrogen): Creatinine = >15:1
- Increased reabsorption of Na+ Urine concentration <20 mEq/L
- Urine very concentrated - >500mosm/kg
- Metabolic acidosis- (decreased clearnce or organic and non organic acids)
- Hyperkalemia (decreased renal excretion of potassium or extracellular shifting of potassium into the blood due to metabolic acidosis
- Hyperphosphatemia- phospohorus can not be secreted by damaged tubules
- Anaemia- Decreased erythropoietin production over weeks
Can also cause platelet dysfucntion causing bleeding and clotting disorders - Fluid overloaed- consequence of oligouria
