Genitourinary Flashcards
what are the 3 classical locations for renal stones to get stuck?
- Ureteropelvic junction
- pelvic brim
- Ureterovesical junction
what are most renal stones made up of? give some other possible constituents
*calcium oxalate.
phosphate, urate, hydroxyapatite, mixed.
give 3 predisposing factors for renal stones
hypercalcaemia, sarcoidosis, hyperparathyroidism, high uric acid, UTI, PKD, loop diuretics, antacids
why do renal stones form?
form when normally soluble material supersaturates the urine.
must also overcome the inhibitors of crystal formation present in normal urine.
what causes calcium renal stones?
hypercalciuria, due to hypercalcaemia - due to e.g. hyperparathyroidism, excess dietary clacium, excessive bone resorption (prolonged immobilisation)
who are particularly at risk of uric acid stones?
those with clinical gout - hyperuricaemia.
those with ileostomies - loss of bicarbonate from GI secretions leads to acid urine, reducing solubility of uric acid.
how might frequent UTIs put you at risk of renal stones?
some infecting organisms produce urease
describe the pain of renal colic
excruciating spasms, ‘loin to groin’.
often with nausea, comes and goes in waves, restlessness, dysuria, desire but inability to void.
what is the best investigation to visualise renal stones with?
KUBXR (kidney, ureter + bladder) or spiral CT
what other investigations might you perform in renal colic?
urine dipstick - 90% +ve for blood.
MSU for MC&S.
24h urine for calcium, oxalate, urate, citrate sodium, creatinine, stone biochemistry
how would you treat a patient with renal stones?
analgesia - diclofenac.
if 5mm - shock wave lithotripsy - US waves shatter stone.
give some examples of steps to be taken to prevent recurrence of renal stones
drink plenty, normal dietary calcium intake, allopurinol for urate stones, pyridoxine for oxalate stones.
define hydronephrosis. what can it lead to?
dilatation of renal pelvis - compression and thinning of renal parenchyma - decrease in kidney size.
what happens to the urinary tract proximal to a point of obstruction?
dilates
give 3 possible causes of urinary tract obstruction
prostatic obstruction - hypertrophy or tumour.
gynaecological cancers.
hypercalcaemia.
caliculi (stones).
renal tubular acidosis.
primary hyperoxaluria.
medullary sponge kidney.
TB.
how would acute upper urinary tract obstruction present?
loin to groin pain.
superimposed infection ± loin tenderness.
enlarged kidney.
how would chronic upper urinary tract obstruction present?
flank pain, renal failure, superimposed infection, polyuria (due to impaired urine concentration).
how would acute lower urinary tract obstruction present?
severe suprapubic pain.
symptoms of bladder outflow obstruction.
distended, palpable bladder, dull to percussion.
how would chronic lower urinary tract obstruction present?
urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence.
distended palpable bladder.
how would you treat upper urinary tract obstruction?
nephrostomy or ureteric stent.
alpha blockers - decrease ureteric spasm, help with stent pain.
how would you treat lower urinary tract obstruction?
urethral/suprapubic catheter.
treat underlying cause.
possible large diuresis on relief of obstruction - watch for salt loss!
give 2 pre-renal causes of AKI
renal hypoperfusion, sepsis, CCF, cirrhosis, renal artery stenosis, NSAIDs, ACE inhibitors
give 2 renal causes of AKI
acute tubular necrosis, PKD, SLE, renal cell carcinoma, myeloma, diabetic nephropathy, drugs, vasculitis, thrombus, HUS, TTP, infections.
give 2 post-renal causes of AKI
urinary tract obstruction by stones/clots, blocked catheter, retroperitoneal fibrosis, benign prostatic hypertrophy/prostatic carcinoma
what would be the most worrying investigation result in AKI?
hyperkalaemia
what is used as a way to estimate kidney function? why is it good for this?
serum creatinine, used to calculate eGFR.
produced by body at pretty steady rate and is excreted by kidneys through glomerular filtration - no reabsorption.
if filtration is impaired, this is shown by high serum creatinine.
serum urea also rises in AKI.
give 3 risk factors for AKI
age >75yrs, CKD, cardiac failure, peripheral vascular disease, chronic liver disease, diabetes, drugs, sepsis, poor fluid intake/increased losses
how would you investigate AKI?
ABCs - asses volume status for C! urgent potassium check for hyperkalaemia.
urine dipstick + MC&S.
renal USS, CT KUB.
renal biopsy.
FIND CAUSE basically.
how would you manage a patient with AKI?
IV fluids.
hyperkalaemia - calcium, glucose and insulin.
stop nephrotoxic drugs - NSAIDs, ACEis etc.
treat cause.
explain the classification of CKD
1 - GFR >90, other renal damage
2 - 60-89, other renal damage
3a - 45-59 ± renal damage
3b - 30-44 ± renal damage
4 - 15-29 ± renal damage
5 - less than 15 - established renal failure
give 3 causes of CKD
diabetes (type 2»type 1).
glomerulonephritis (IgA nephropathy, SLE, vasculitis).
idiopathic, hypertension, renovascular disease, pyelonephritis, reflux nephropathy, PKD.
give 3 risk factors for CKD
diabetes, hypertension, heart disease, smoking, obesity, age >65yrs, FHx
give 3 symptoms of CKD
fatigue, weakness, anorexia, vomiting, metallic taste, pruritus, restless legs, bone pain, impotence
give 3 signs of CKD you might find on examination
uraemic flab, leuconychia, scratch marks, raised JVP, anaemia, ascites, peripheral neuropathy, AV fistula
what lifestyle measures would you ask a CKD patient to take?
stop smoking, lose weight, exercise, sodium restriction, increase fluid intake
how would you medically manage CKD?
stop nephrotoxic drugs, tight glucose control.
ACEi or ARB to target BP less than 140/90
explain how haemodialysis works
blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction - small solutes diffuse down this concentration gradient into the dialysis fluid.
how can haemodialysis be used to clear excess fluid?
ultrafiltration, to create a negative transmembrane pressure, clearing fluid from the blood
give 2 problems with haemodialysis
risk of disequilibration syndrome, hypotension, time consuming.
access problems - need AV fistula or tunnelled venous access line
explain how haemofiltration works
blood is filtered across a highly permeable membrane, allowing movement of small and large solutes by convection.
ultrafiltrate is replaced with an equal volume of fluid.
what is the main problem with haemofiltration?
takes a lot longer than haemodialysis - useful in critically ill patients, but impractical long term
explain how peritoneal dialysis works
uses the peritoneum as a semi-permeable membrane - catheter is inserted into the peritoneal cavity and fluid infused. sits in the cavity, allowing solutes to diffuse across.
what are the main positives and negatives of peritoneal dialysis?
positives - can be carried out at home, ‘ambulatory’ PD can be used, or overnight, so patient leads normal life.
negatives - peritonitis, exit site infection, loss of membrane function over time, herniation at exit site.
give 2 contraindications to renal transplantation
active infection, cancer, severe comorbidity
give 2 possible complications of renal transplantation
surgical - bleed, thrombosis, infection, hernia.
delayed graft function, drug toxicity, infection, malignancy, rejection.
how would you manage acute rejection of a kidney transplant?
high dose IV methylprednisolone + intensify immunosuppression regime.
what 2 genes are associated with ADPKD and what is the difference between them?
PKD1 and PKD2.
PKD2 renal cysts develop more slowly - ESRF comes later.
give 3 signs of ADPKD
renal enlargement with cysts.
abdo pain ± haematuria (haemorrhaging cyst).
cyst infection, renal caliculi, hypertension, progressive renal failure.
name 2 extra-renal features of ADPKD
liver cysts, intra-cranial aneurysm leading to subarachnoid haemorrhage, mitral valve prolapse, ovarian cysts, diverticular disease
how would you treat a patient with ADPKD?
aggressive BP management (less than 130/80)
how would you diagnose ADPKD?
renal USS.
screen family members using USS too.
what is the difference between ADPKD and ARPKD?
autosomal recessive is an infancy disease with renal cysts and congenital hepatic fibrosis
define nephritic syndrome/glomerulonephritis
group of disorders where damage to the glomerular filtrating apparatus causes leaking of protein/blood into the urine.
common cause of ESRF.
give 3 causes of glomerulonephritis
SLE, infections (strep throat, HIV), vasculitis, gold, penicillamine, malignancy of breast/bone/myeloma, diabetes, hypertension
what investigation would you perform in glomerulonephritis?
renal biopsy
what lung disease is associated with a type of glomerulonephritis?
Goodpasture’s syndrome aka anti-glomerular basement membrane disease
explain the pathology of IgA nephropathy
patient starts with sore throat/UTI due to streptococcus - triggers an immune reaction, leading to deposition of IgA complexes in the glomeruli
what would a biopsy show with rapidly progressive glomerulonephritis?
crescents
how would you treat a glomerulonephritis, other than treating the underlying cause?
methylprednisolone + cyclophosphamide.
control BP with ramipril + losartan.
how does IgA nephropathy usually present?
with macroscopic/microscopic haematuria (occasionally with nephritic syndrome)
what are the features of nephrotic syndrome?
normal/mildly high BP.
urine = proteinuria.
GFR = normal to mildly low.
what are the features of nephritic syndrome?
BP = moderately/severe high.
urine = haematuria.
GFR = moderate to severely low.
what is seen on renal biopsy in IgA nephropathy?
mesangial proliferation, IgA and C3 deposits
what is Henoch-Schonlein purpura? how does it present?
systemic variant of IgA nephropathy - causes small vessel vasculitis.
purpuric rash on extensor surfaces, flitting polyarthritis, abdo pain, nephritis.
how would you diagnose Henoch-Schonlein purpura?
IgA and C3 deposits seen in renal or skin biopsy
what parts of the kidney are damaged in SLE?
vascular, glomerular and tubulointerstitial components
how would you diagnose anti-GBM disease (Goodpasture’s)?
serum anti-GBM - autoantibodies to type IV collagen (in GBM)
give some different causes of rapidly progressive glomerulonephritis. what do they all have in common?
all show crescents affecting most glomeruli at biopsy.
immune complex disease e.g. post infection, SLE, IgA/HSP.
Pauci-immune disease (ANCA+ve) - granulomatosis with polyangitis (Wegener’s), microscopic polyangitis.
Goodpasture’s.