RENAL Flashcards
pre-renal causes of AKI
reduced renal perfusion (fluid depletion/dehydration, sepsis, renal artery obstruction, reduced cardiac output)
post-renal causes of AKI
stones, tumours, BPH, obstruction in bladder/ureters/urethra
intra-renal causes of AKI
acute tubular necrosis, interstitial nephritis, vasculitis, GN, renal artery/vein obstruction
sings of AKI
hyperkalaemia/hypokalaemia raised creatinine raised urea acidosis reduced/no urine output
examples of fluid shift
ascites, effusions, capillary leak states (sepsis/burns)
causes of negative fluid balance
decreased input
increased output
fluid shift
renin is secreted in response to what
reduction in glomerular filtration rate
how is a reduction in the GFR detected
stretch receptors in the macula dense cells of the juxtaglomerular apparatus are stimulated
action of renin
angiotensinogen to angiotensin I
which enzyme converts angiotensin I to angiotensin II
ACE
what stimulates release of aldosterone
renin
effect of aldosterone release
increased sodium reabsorption in the DCT
increased excretion of potassium
what is renal artery stenosis
narrowing of the renal artery lumen
chronic elevation of angiotensin II results in what
cardiac and vascular hypertrophy
what does atrial natriuretic factor detect
atrial filling
what stimulates release of ANP
increased volume (increased atrial filling)
what does ANP do
inhibits sodium reabsorption in the DCT (opposes aldosterone)
mechanism of action of ACEIs
inhibits the formation of angiotensin II leading t vasodilatation
examples of ACEI
rampiril, lisonopril
mechanism of action of ARBs
block angiotensin II receptors on blood vessels/tissues
examples of ARBs
losartan
actions of ACEIs/ARBs on the CV system
dilate arteries (reduce arterial pressure, preload and after load) down regulate sympathetic adrenergic activity promote renal excretion of Na and water (reduces blood volume, venous pressure and arterial pressure) inhibit cardiac and vascular remodelling associated with HTN, HF, MI
mechanism of action of a1 receptor blockers
block a1 adrenoceptors in the bladder and prostate, relaxing smooth muscle and reaching resistance to urinary flow and damage to kidneys from downstream obstruction
example of a1 receptor blocker
tamulosin
nephrotoxic side effects of gentamicin
acute tubular necrosis
nephrotoxic side effects of vancomycin
acute interstitial nephritis
nephrotoxic side effects of ACEIs
reversible acute renal failure (HTN/CHF)
nephrotoxic side effects of diuretics
reduced GFR
hypokalaemia nephropathy
polyuria
interstitial nephritis
nephrotoxic side effects of NSAIDs
AKI caused by sodium and water retention, reducing renal blood flow and direct kidney injury
what is the ‘triple whammy’ effect
the significant increase in harm that may result from the combined use of NSAIDs, ACEIs/ARBs and diuretics in high-risk individuals.
mechanism of action of the ‘triple whammy’ effect
NSAIDs constrict the blood flow into the glomerulus via the afferent arteriole by inhibiting vasodilator prostaglandins
ACEIs/ARBs decrease angiotensin II level/action, leading to reduced GFR by dilating the efferent arteriole
diuretics induced dehydration and blood volume reduction leading to insufficient renal haemodynamics and failure to maintain GFR
what is the definition of CKD
gradual loss of kidney function due to abnormal function or structure
what is the best measure of overall kidney function
GFR
what factors are taken into account when calculating eGFR
serum creatinine, age, gender, race
what advice should be given to patients before eGFR testing
avoid eating meat for 12 hours before
GFR for CKD stage 1
> 90
GFR for CKD stage 2
60-89
GFR for CKD stage 3
30-59
GFR for CKD stage 4
15-29
GFR for CKD stage 5
<15
effect of ageing on GFR
decreases with age
NICE guidance for patients over 70 with reduced GFR
stable GFR >45 is unlikely to be associated with CKD-related complications
GFR for CKD stage 3A and 3B
3A 45-59
3B 30-44
what does the suffix P mean in relation to CKD staging
proteinuria
common causes of CKD
diabetes, GN, pyelonephritis, renal vascular disease, polycystic kidney disease, hypertension
patients at higher risk of developing CKD
diabetics hypertension CVD structural renal tract disease multi system disease with potential for renal involvement (eg SLE) patients with a FH of CKD stage 5
common nephrotoxic drugs
NSAIDs
lithium
diuretics
ACEIs
lifestyle measures for management of CKD 1,2,3
smoking cessation weight loss regular exercise and a healthy diet sensible alcohol consumption low salt
what is classed as progressive CKD
decline of more than 5 ml/min/1.73m^2 over 1 year OR more than 10 ml/min/1.73m^2 over 5 years
how often should BP be measured in patients with CKD
at least once a year
BP target s for patients with CKD
120-139 mmHg systolic and <90 mmHg diastolic UNLESS proteinuria/diabetic with microalbuminuria 120-129 mmHg systolic and <80 mmHg diastolic
recommended lab testing for CKD stage 1/2
eGFR, PCR/ACR yearly
recommended lab testing for CKD stage 3
eGFR, PCR/ACR, Hb, K+, Ca2+, phosphate 6 monthly (12 monthly if stable)
recommended lab testing for CKD stage 4
eGFR, PCR/ACR, Hb, K+, Ca2+, phosphate, HCO3, PTH 3 monthly
recommended lab testing for CKD stage 5
eGFR, PCR/ACR, Hb, K+, Ca2+, phosphate, HCO3, PTH 6 weekly
first line management of HTN (protein/microalbuminuria) in CKD
ACEIs (or ARBs)
when should ACEIs be reduced in dose or stopped
if there is more than a 25% fall in eGFR from the pre-ACEI value
indications for referral to nephrologist in CKD
acute renal failure
malignant hypertension
hyperkalaemia (>7 mmol/L)
nephrotic syndrome
what is renal bone disease
CKD is associated with elevated PTH, in association with low Ca and high phosphate, and inadequate renal vitamin D production
what type of anaemia is commonly associated with CKD
normochromic normocytic anaemia
what causes anaemia in CKD
inadequate production of erythropoietin
risk factors for urinary incontinence
female sex pregnancy vaginal delivery pelvic surgery pelvic organ prolapse raised IAP (chronic constipation, lung disease) obesity menopause caffeine
incontinence may be caused by
neurological dysfunction
abnormalities of detrusor function
abnormalities of the sphincter apparatus (including surrounding pelvic floor muscles and tissue)
anatomical abnormalities
four main types of incontinence
stress
urge
mixed
overflow
what is stress incontinence
leakage of urine caused by effort or exertion or on coughing/sneezing
causes of stress incontinence
problem with the sphincter apparatus
neurological problem
what causes urge incontinence
overactivity of the detrusor muscle
what is urge incontinence
uncontrollable leaking of urine preceded by or accompanied by a sudden urge to void
what is overflow incontinence
large volume chronic retention due to bladder outflow obstruction resulting in leaking when the bladder can hold no more urine
what causes overflow incontinence
prostatic enlargement
bladder obstruction
complications of overflow incontinence
associated with increased risk of renal failure due to vesicouteric incompetence and hydrostatic pressure on the renal system
triggers for stress incontinence
coughing, sneezing, exercise, lifting or rising from sitting
tiggers for urge incontinence
running taps
cold weather
examination of incontinence
abdominal exam
PR (men)
pelvic (women)
neurological
investigations of incontinence
bladder diary for three days
urine dip
bladder scan
management of stress incontinence
pelvic floor exercises
recommend weight loss
management of urge incontinence
bladder training (6 weeks) oxybutynin if ineffective intravaginal oestrogen if atrophy recommend decreased caffeine intake and weight loss
urgent referral criteria for incontinence
non-visible haematuria if over 50
visible haematuria in any age group
recurrent/persistent UTI with non-visible haematuria if over 40
suspected levin mass
routine referral for incontinence
prolapse of the vagina that is symptomatic and visible
patients with a palpable bladder after voidinh/high post-void volume
consider referral for incontinence
persistent bladder/urethral pain
associated faecal incontinence
suspected neurological disease
voiding difficulties
suspected fistula (continuous incontinence)
previous surgery to correct incontinence
previous pelvic irradiation/cancer surgery
surgical management of stress incontinence
mid-urethral tapes such as tension/free vaginal tapes or transobturator tapes
secondary care management of urge incontinence
botox injections
sacral nerve stimulator