RENAL Flashcards
(36 cards)
Nephrotoxic drugs
Pre renal:
- NSAIDS
- ACEi
- cyclosporine/ tacrolimus
Intrinsic
ATN
- aminoglycosides (genta/ amikacin)
- Contrast
- amphotericin B
- cisplatin
AIN
- thiazides
- beta lactams/ penicillins
- allopurinol
- sulphonamides
Post renal cyst forming
- aciclovir
- methotrexate
- sulfonamides
causes of pre renal AKI
reduced perfusion
- hypovolaemia
- sepsis
- major haemorrhage
causes of intrisic AKI
nephrotic
nephritic
ATN
lupus nephritis
Iatrogenic- aminoglycosides, contrast, cisplatin
causes of obstructive AKI
any growth obstructing urinary tract
- prostate hyperplasia
- gynae malignancy/ fibroids
- GI growth
indications for dialysis
symptomatic uraemia
refractory acidosis (ph <7.1)
severe hyperkalaemia not responding to medical Mx
ESKD (stage 5)
refractory fluid overload
Drugs that can cause an AKI
ACEi- vasodilation of efferent arterioles and renal artery stenosis
Aminoglycosides eg. gentamycin and amikacin- acute tubular necrosis
tacrolimus- toxicity-pre renal AKI causing vasoconstriction of afferent arteriole. chronic tacrolimus causing intrinsic nephrotoxicity
how to prevent and minimise AKI
minimise duration of administration
narrow therapeutic drug monitoring by monitoring serum drug levels
appropriate renal drug dosing based on eGFR
closely monitor renal function
stages of an AKI
stage 1- increased serum Cr > 26umol/L within 48 hrs, <0.5mls/kg/hr urine output
stage 2
stage 3
red man syndrome
when given vancomycin too quickly
allergic reaction and AKI
drugs to withold if pt in AKI
CANADA
contrast
aminoglycosides
NSAIDs
Diuretics
ACEi
what drugs is a pt with CKD requiring haemodialysis most likely be on
antiplatelets eg. clopidogrel and aspirin
synth EPO injections
alfacalciferol
SGLT2 inhibitor eg. dapaglifozin
PPI H+ inhibitors (uraemia can predispose to GI ulcers)
?allopurinol
what would you expect in terms of insulin requirements in a dialysis pt
insulin requirements lower in a dialysis pt as the dialysis only clears small molecules, insulin is too big to be cleared so remains in the system longer
CKD A-I assessment
A- Anaemia: inadequate secretion of EPO
B- Bone: vit D def, low Ca, high phos, 2/3 hyperparathyroidism
C- Cardiovascular disease: anticoag eg. LMWH, lipids, BP + diabetes
D- Dialysability of drugs/ soluble vitamins (DEK vits all removed) (be mindful of how much of a drug is dialysed)
E- Electrolytes. Na, K, H+, Phos
F- fluid balance. intake/output , diuretics vs dialysis, urinary sx, proteinuria
G- GI disturbances (nausea and loss of appetite post dialysis). Gout from build up of uric acid.
H- How renal failure affects response to drug
I- Infection prophylaxis
what is calciphylaxis
calcification of blood vessels in the skin
warfarin can also cause
describe where a tesio line goes
central line to Internal Jugular and RA, tunnelled under skin and has 2 lumens entering skin
difference between a tesio and a Swan-Gantz line
tesio- 2 lumens
S-G- 3 lumens
what is Dialysis Disequilibrium Syndrome
The dialysis disequilibrium syndrome (DDS) is characterized by a range of neurologic symptoms that affect patients on hemodialysis, particularly when they are first started on dialysis [1,2]. However, it is also seen among patients who have missed multiple consecutive dialysis treatments.
symptoms are thought to be as a result of CEREBRAL OEDEMA
Which immunosuppressants are commonly used in a post renal transplant?
calcineurin inhibitors eg. tacrolimus
anti proliferative- Mycophenolate motefil/ azathioprine
steroids
Work up of things to think about if someone is showing signs of an AKI
STOP
Sepsis/ dehydration
Toxins (ACEi, Abx, NSAIDs, contrast)
Obstrustion
Parenchymal disease
Classify the stages of an AKI
Standardised definition of AKI (KDIGO): Serum Creatinine (70-100) UO
o AKI Stage 1: Increase ≥26 µmol/L; or by 1.5-1.9x the reference sCr <0.5mL/kg/hr, 6-12hr
o AKI Stage 2: Increase 2.0-2.9x the reference sCr <0.5mL/kg/hr, ≥12hr
o AKI Stage 3: Increase ≥354 µmol/L; or by ≥3x the reference sCr <0.3mL/kg/hr, ≥24hr
Anuric for ≥12hr
Consequences of CKD
endocrine function:
Anaemia due to reduced EPO production
renal bone disease due to decreased activation of 1ahydroxylase
Cardio:
renal vascular calcification- renal osteodystrophy
Homeostasis:
Hyperkalaemia
acidosis
Uraemia / encephalopathy
signs and symptoms of IgA nephropathy
Signs & symptoms:
· Purpuric Rash (100%)
o Extensor surface of legs, arms, buttocks, ankles
o Urticarial: maculopapular; spares trunk
· Arthralgia and periarticular oedema (60-80%):
o Large Joints
o Joint pain and swelling of knees and ankles
· Abdominal pain (60%)
o Colicky abdominal pain
o Haematemesis, melena, intussusception
· Glomerulonephritis (20-60% à 97% within 3m of onset) – U&Es typically NORMAL:
o Microscopic or macroscopic haemat
Investigations for IgA nephropathy
· 1st: FBC, clotting screen, urine dipstick, U&Es
· Urinalysis: RBCs, proteinuria, casts, urea, creatinine, 24hr protein à rule out meningococcal
· Increased IgA, normal coagulation
· Follow-up (weekly for 1 month, 2-weekly for 2 months, 3 months, 6 months, 12 months):
o BP measurements
o Urine dipstick (haematuria)
Urine microscopy:
Hyaline casts
- Consist of Tamm-Horsfall protein (secreted by DCT)
- Seen in normal urine, after exercise, during fever or with loop diuretics
