Revision Flashcards
what is the classical presentation of bladder cancer
painless frank haematuria, may be intermittent as bladder contracts and voids
what cancer will an ultrasound miss
transitional cell carcinoma of the collecting system of the ureter
what usually causes painful frank haematuria
infection or renal stone
what investigations for frank haematuria
always requires a cystoscopy and at least one mode of upper urinary tract imaging (IVU or renal ultrasound)
does renal and bladder cancer cause intermittent or constant haematuria
intermittent
what are the defences against getting an STI
Immune system, acid in periurethral tissues (post-menopausal women have a change in these pH), length of the urethra (4cm) makes it more vulnerable than men to infections, urothelium (if this is damaged more vulnerable to infection)
what might recurrent UTIs in childhood suggest
anatomical abnormality
who is at risk of UTIs
Elderly (in BPH there is a post void residue where bacteria can replicate), catheterised, diabetics, immunocompromised, abnormal urinary tract anatomy, renal calculi, stents
what can help prevent UTIs
Drinking lots, avoid perfumed products, voiding after intercourse
what can you give for frequent UTIs
prophylactic antibiotics for a few months, bladder instillations
why are you more susceptible to UTIs when you are pregnant
get mild hydronephrosis and dilation of upper urinary tract, may get gestational diabetes
what are the symptoms of polynephritis
constant ache in relation to fever
what antibiotic for complicated UTI in men and women
men- trimethoprin (dont give in renal impairment)
women- nitroflutonin
how do stones affect youre chance of getting an infection
increase likely hood of it
what organisms are associated with kidney stones
proteus organisms
how does incomplete voiding affect chances of UTI
increases them
what is nocturnal polyuria
Producing more urine that normal during the night (affects men and women) e.g. cardiac failure (diagnose with urine diary)
what is enuresis
wetting the bed
what are the voiding symptoms
hesitancy, poor flow, incomplete voiding
what are the storing symptoms
frequency and urgency
what does a palpable bladder suggest
urinary retention
what is PSA a marker for
(prostate specific antigen)
raised in prostate cancer
can be normal in prostate cancer
also raised in BPH, stones, catherterisation (+ anything that causes prostate inflammation)
what is the treatment for BPH
Alpha blockers, anti cholinergics (if they have urgency), 5- alpha reductase inhibitors, then surgery
what are the three types of AKI
pre renal
renal
post renal
what causes a pre renal AKI
hypovolaemia (haemorrhage, burn, D&V, diuresis)
oedema (CHF, cirrhosis, nephrotic syndrome)
hypotension
cardiac problems (failure, arrhythmias)
renalhypoperfusion (NSAIDS, ACEi, ARBs, AAA, renal artery stenosis/ occlusion, hepatorenal syndrome, sepsis)
what can cause renal AKI
glomerular disease (GN, thrombosis, HUS)
tubular injury (acute tubular necrosis following prolonged ischaemia, nephrotoxins- aminoglycosides (gentamicin), contrast, myoglobin, cisplatin, metals, light chains in the kidney)
acute interstitial nephritis due to drugs (NSAIDs), infection or autoimmune diseases
vascular disease (vasculitis, renal artery/vein stenosis, malignant hypertension)
eclampsia
what can cause a post renal AKI
calculus, blood clot, papillary necrosis, urethral stricture, prostatic hypertrophy/ malignancy, bladder tumour, radiation fibrosis, pelvic malignancy
what are the clinical markers of an AKI
decreased urine output (less than 0.5 mL/kg/hr for more than 6 hours)
and a rise in serum creatinine (26 micromol/L within 48 hrs/ 50% increase within 7 days)
what are the symptoms of an AKI
urine output: abrupt anuria= acute obstruction, acute and severe GN, acute renal artery occulsion. gradual decrease= urethral stricture, bladder outlet obstruction. nausea, vomiting, diarrhoea confusion hypertension dehydration palpable bladder fluid overload, oedema pericardial rub (pericarditis due to uraemia)
what investigation for post renal AKI
USS to see size, obstruction, hydronephrosis
what is the treatment for hydronephrosis
put in catheter to relieve pressure then nephrostomy or stent to treat obstruction
if you have an AKI with blood and protein in your urine what is the most likely type of AKI
renal
is furosemide nephrotoxic
no but can injury kidneys if given when patient already dehydrated
what can increase urea in a GI bleed
digestion of blood
what treatment for a peptic ulcer bleed
IV PPI infusion
use blecthford score to see what treatment needed
inject adrenaline to vasoconstrict during endoscopy
how does ibruprofen affect the kidneys
inhibit prostaglandins causing vasoconstriction, decreasing blood supply to kidney,= acute ischaemic necrosis
what is the normal potassium range
3.5-5.3
what is the treatment for hyperkalaemia
Give 10ml calcium gluconate 10% intravenously. This doesn’t lower
serum potassium, but protects the heart against arrhythmias.
Give 10 units Actrapid insulin with 50ml glucose 50% intravenously.
Insulin causes potassium to move into cells. Glucose must be given
with insulin to prevent hypoglycaemia, and blood glucose level
monitored.
Give 2.5mg salbutamol by nebuliser. β-agonists also cause potassium
to enter cells.
what ECG for hyperkalaemia
tall tented t waves (look sore to sit on) and broadened QRS
what are the indications for dialysis
hyperkalaemia refractory to Tx
acidosis
pulmonary oedema which is refractory to diuretics
uraemia
what are the possible complications of ureamia
uraemic pericarditis
uraemic encephalopathy
what vasculitis: pulmonary renal syndrome with signs of a pulmonary haemorrhage
good pastures
pulmonary renal syndrome= bleeding in lungs and glomerulonephritis
when would you give plasma exchange in vasculitis
if they have pulmonary haemorrhage and vasculitis
what is the treatment for goodpastures
cyclophosphamide initially then azathiprine/ MMF as maintenance
what makes up the myeloma screen
immunoglobulin levels, serum protein electropharesis, complement, bence jones protein
what is first line therapy for patients with hypertension and CKD
ACEi
what warning should be given with ace inhibitors
they are teratrogenic
can you give an ice inhibitor in bilateral renal artery stenosis
no will cause further vasoconstriction and hypoperfusion
what medication for urge incontinence
oxybutin- (antimuscarinic)
what drug for stress incontinence
duloxetine if pelvic floor exercises not working
what is the usual presentation of adult polycystic kidney disease
usually in middle age, sometimes in young adults
may present with features of chronic renal failure, an abdominal mass or a subarachnoid haemorrhage
where does the haemorrhage usually occur in PKD
rupture of a berry aneurysm in the circle of willis
why do you get LVH in PKD
systemic hypertension as a result of chronic renal failure
where else can you get cysts in PKD
pancreas, liver, lung (doesnt usually affect function)
what inheritance is PKD
AD- short arm of chromosome 16 (tubuloscelrosis)t
is PKD in children AD or AR
AR (much more severe)
how can glomerular disease present
haematuria (macro or micro)
proteinuria
acute nephritic syndrome (= oliguria, haematuria, dusky coloured urine, mild facial oedema)
nephrotic syndrome (= hypoalbuminaemia, pitting oedema, hypercholesterolaemia)
renal failure (acute/ chronic- chronic may present as hypertension)
what is epithelial cresent formation
manifestation of severe glomerular damage
proliferation of the epithelial cells in bowans capsule causes compression and distortion of the glomerular tuft
what is glomerular scelrosis
complete and irreversible
end stage process in severe glomerular disease
what is the other name for acute diffuse proliferative GN
post infectious
what is the difference between membranous GN and membranoproliferative
membranous= nephrotic, non proliferative, complement deposition in the basement membrane causing it to thicken with spikes
membranoproliferative- nephritic. nephrotic, proliferative, tram track membranes (big lobulated hypercellular glomeruli with thick memebranes)
what is the difference between post infectious and IgA GN
IgA- IgA deposits on mesangium, macroscopic haematuria few days after infection (URTI)
post infectious- nephritic, several weeks after infection
what GN is associated with cresents
rapidly progressing GN (caused by vasculitis)
what is the buzzword for histological sign for diabetic nephropathy
kimmel stiel wilson nodule
what are the renal manifestations of myeloma
glomerular- AL amyloidosis, immunoglobulin (heavy/light chain) deposition
tubular - light chain cast nephropathy
congo red stain, apple green birefringence=
amyloid
what can cause amyloid deposition
myeloma, RA, chronic inflammatory conditions
is a seminoma radio or chemo sensitive
radio sensitive
what is PLAP
placental alk phos- tumour marker for seminoma
is AFP used as a seminoma tumour marker
no produced by yolk sac non seminoma
what is different about mets of prostatic carcinoma
they are sclerotic lesions (most mets to bone are lytic)
what is malignant hypertension
a hypertensive emergency where a recent increase in BP causes organ damage (encephalopathy, cardiovascular or renal)
in malignant hypertension there is papiloedema
what causes a hypertensive emergency (accelerated/ malignant hypertension)
renal artery stenosis renin secreting tumour kidney trauma renal vasculitis phaeochromocytoma cocaine pre eclampsia hyper/hypo thyroidism
what is the presentation of a hypertensive emergency (accelerated/ malignant)
headache fits n&v chest pain visual disturbance cardiac failure haematuria papilloedema and retinal haemorrhages
what are causes of secondary hypertension
Renal artery stenosis (can cause flash pulmonary oedema), Diabetic nephropathy, glomerular disease, PKD, renovascular disease. Any thing that causes kidney damage can cause hypertension
what is pevicalyceal dilation
hydonephrosis
what are the complications of renal calculi
Loin to groin pain, haematuria, dysuria, UTI, urinary obstruction, AKI
how do you quantify proteinuria
protein: creatinine ratio / measure protein in a 24 hr urine collection
what are the features of nephrotic syndrome
proteinuria, hypo-albuminaemia, oedema, hyperlipidaemia
what usually presents with nephrotic syndrome, normal renal function and BP
minimal change GN, membranous GN
what is primary GN
GN with no underlying disorder
what drugs can cause GN
gold, penicillamine
what tests need to be done before a biopsy is done
blood count and coagulation screen
renal USS to check that two kidneys are present and the size and position of the kidneys
what are the contraindications to a renal biopsy
clotting abnormalities
small kidneys (increased risk of bleeding, scarred biopsy is uninformative)
uncontrolled hypertension (bleed)
untreated urine infection (2nd haemorrhage 10 days after biopsy)
presence of a single kidney (not absolute contraindication)
what treatment for minimal change GN
prednisolone strarting at 40-60 mg daily
PPI to protect against peptic ulceration
what is the prognosis of minimal change nephropathy
good
renal function shouldn’t deteriorate
responds well to steroids
if relapse then may need further steroids/ immunosuppressive drugs
why do you get low potassium in nephrotic syndrome
losing protein in urine
water follows protein
aldosterone and ADH stimulated to retain water
cause hypernatraemia and hypokalaemia
how can you confirm IgA nephropathy diagnosis
renal biopsy
what is seen in urinalysis in IgA GN
haematuria and proteinuria
what 2 things do ACE inhibitors help with
reducing hypertension
reduce proteinuria
what is the prognosis of IgA GN
Many patients with IgA nephropathy maintain good renal function indefinitely, but in about 25%, renal function progressively declines, and eventually dialysis or transplantation is required.
v important to control BP and proteinuria (via ACi)
what are poor IgA prognostic markers
heavy proteinuria
sclerosis and interstitial scarring
where is the most likely source of isolated haematuria (no proteinuria) in young and old patients
young= kidneys old= bladder
what happens when there is prolonges renal hypoperfusion
acute tubular necrosis
why does rhabdomyolysis and haemolysis cause acute renal fialure
(large destruction of skeletal muscle)
haemoglobin and some products of muscle breakdown are toxic to renal tubules
what are the complications of ARF
hyperkalaemia, metabolic acidosis, fluid overload
what will most kidneys in CKD be like of USS
small
what are the stages of CKD
1- normal/ increased GFR (>90) with evidence of kidney damage 2- 60-90 with kidney damage 3- 30-60 4- 15-30 5- GFR< 15/ on renal replacement therapy
what is evidence of kidney damage
proteinuria, abnormalities on scanning
what risk increases as GFR decreases
cardiovascular risk
when do you start to get symptoms of reduced GFR
when under 20
what groups are more likely to get CKD
diabetes, hypertension, heart failure
how do you screen high risk patients for CKD
urinalysis; proteinuria increases the risk of progression of CKD;
haematuria may indicate renal disease or a lesion of the lower urinary tract.
If proteinuria is present, quantify by sending a urine sample for
measurement of protein:creatinine ratio (PCR). A ratio of 100mg/mmol is
approximately equivalent to 1G per day protein excretion.
Decide whether referral to Renal Clinic is necessary
treat CV risk factors
what are the indications for referral to renal unit
nephrotic syndrome Stage 3 CKD with urine PCR >100mg/mmol Stage 3 CKD with progression (GFR falling by >20% over 6 months) Stage 3 CKD in younger people (age <60) Stage 4 CKD Haematuria (after exclusion of ‘urological’ causes in older patients)
what can you hear over femoral arteries in peripheral vascular disease
bruits
in someone with peripheral artery disease and reduced kidney function what should you worry about
renal artery stenosis
what will USS show in renal artery stenosis
small irregular kidneys (damaged by the ischaemia)
should you do CT/MR angiogram in renal stenosis
no as can tubuar toxicity of scan can cause intra arterial contrast induced nephropathy
what treatment for hypertension retinopathy with suspected renal artery stenosis
CCB and alpha blocker (doxazozin)
dont use ACEi in renal artery stenosis as cause cause AKI in renovascular disease
do you give ACEi/ ARB in renovascular disease
no will cause AKI
when is the peak incidence for contrast induced nephropathy
48-72 hrs after the procedure
how can the risks contrast induce nephropathy be reduced
give fluids before and after procedure
what is the treatment for hyperkalaemia
IV calcium gluconate 10 mls 10% over 2-3 mins, 10 units of insulin dextrose 50% in 50 mls, nebulised salbutamol
what causes kidney damage in diabetes
retention of fluid due to high glucose cause increase in circulating volume= increase in kidney perfusion
= a hyperfiltration injury - high flow through the kidneys injures the glomerulus
(a microvascular complication)
when might a renal biopsy be indicated
when there is blood in urine, abnormal antibody tests
how do you evaluate anaemia
iron, folate, B12, blood film for erythropoietin levels, measure thyroid levels, FBC
what is the treatment for anaemia in CKD
erythroietin injections, iron supplements
what can happen to phosphate and PTH in CKD
get high phosphate as not clearing it effectively which causes a rise in PTH
how do you treat high phosphate and PTH in CKD
reduce phosphate will a low phosphate diet or phosphate binders
if phosphate lowered nut PTH still high can give activated for of vit D = alfocalcidol
what can you give if bicarb low
sodium bicarbonate
