urinary Flashcards

1
Q

what is obstructive uropathy?

A

structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction

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2
Q

what are 3 epidemiological facts relating to obstructive uropathy

A
  • 5/10 000 to 5/1000 depending on cause
    Bimodal distribution (2 different age group distributions 2 different age groups it occurs)
    In kids, mainly congenital
    After 60 years, incidence increases particularly in men (BPH [benign prostate hypertrophy], Prostate cancer)
    4% of end stage renal disease
    Hydronephrosis is found in 2-4% of patients
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3
Q

what is the aetiology of obstructive uropathy in kids

A

anatomic abnormalities like stricture, stenosis or valve issues

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4
Q

what is the aetiology of obstructive uropathy in young adults

A

calculi

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5
Q

what is the aetiology of obstructive uropathy in older patients

A

BPH, tumours, calculi

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6
Q

what is the pathophysiology of obstructive uropathy

A

Dilation of the collecting ducts and distal tubules
Chronic tubular atrophy with little glomerular damage
Dilation takes 3 days from the onset of obstructive uropathy to develop; before then, the collecting system is relatively noncompliant and less likely to dilate
Obstructive uropathy without dilation can also occur when obstructive uropathy is mild and renal function is not impaired, and in the presence of an intrarenal pelvis

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7
Q

what are some clinical signs and symptoms of obstructive uropathy?

A
Less likely in chronic obstruction
May include pain radiating to the T11 to T12 dermatomes Abnormal voiding 
Fever
Oedema
Haematuria
Infection i.e. pyelonephritis
Acute flank pain
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8
Q

what are some laboratory findings of obstructive uropathy

A
Urinalysis  
Serum electrolytes 
Creatinine 
Blood urea nitrogen (BUN) 
Bladder catheterisation
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9
Q

what imaging modalities are used when imaging obstructive uropathy

A
MCU/cystogram
X-ray/KUB
Abdominal ultrasound
Doppler ultrasound
CT
pyelogram/ IVP
MRI
Renogram
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10
Q

when is MCU/Cystogram utilised in obstructive uropathy imaging

A

Shows reflux (scarring) and indicates pyelonephritis
Including obstruction; torturous ureters
Anatomy
Usually only if stricture in adult suspected

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11
Q

when is x-ray/ KUB utilised in obstructive uropathy imaging what are some positives and negatives

A

Often first imaging test for flank pain
May demonstrate calculi
Calculi can have varying appearances based on size, composition, location of stones
High degree of false positives and false negatives

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12
Q

when is abdominal ultrasound utilised in obstructive uropathy

A
  • imaging test of choice
  • aimed at detection of hydronephrosis

***Not doing this test to check for hydronephrosis. Do it to say this patient has all signs + symptoms for some sort of obstructive uropathy, let’s do a test to see if they have a stone or not.

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13
Q

positives and negatives of abdo ultrasound in obstructive uropathy

A

False-positive rate is 25% if only minimal criteria (visualization of the collecting systems) are considered in the diagnosis: normal variant for them
Absence of hydronephrosis (and false-negative results) can occur if obstruction is early (in the first few days) or mild

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14
Q

when is doppler us utilised in obstructive uropathy imaging

A

Can usually show unilateral obstructive uropathy in the first few days of acute obstruction before the collecting system dilates by detecting an increased resistive index (a reflection of increased renal vascular resistance) in the affected kidney
Useful in obesity and in bilateral obstruction

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15
Q

when is CT utilised in obstructive uropathy imaging

A

Only use CT if there is a distinct advantage over another modality due to the high radiation dose

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16
Q

positives of CT in obstructive uropathy

A
  • Is sensitive for diagnosing obstructive nephropathy
  • Unenhanced helical CT is the modality of choice for obstruction due to ureteral calculi: anatomic detail
  • CT urography done with and without contrast is particularly useful in the evaluation of haematuria
  • Thinning of the renal parenchyma suggests more chronic obstruction
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17
Q

why isn’t pyelogram/ IVP utilised in obstructive uropathy imaging

A
  • High dose
  • Not functional persee
  • Need to be during symptoms
  • Hard to justify with CT and renography
18
Q

when is MRI utilised in obstructive uropathy imaging

A
  • Anatomy
  • Avoids radiation in kids or pregnant women
  • Inferior for detecting calculi (to CT and US)
  • Inferior to renography for function
  • But nice soft tissue and “water map”
19
Q

When is a renogram with 99mTc-DTPA or 99mTc-MAG3 utilised for obstructive uropathy imaging

A

clinical indications:

  • Quantification of split renal function in either surgical planning or follow-up
  • Serial examination of renal function in patients with an established clinical diagnosis i.e. patients with renal dysfunction, renal transplants, and significant previous reactions to iodinated contrast media
20
Q

When is a renogram with Diuresis (Lasix) utilised for obstructive uropathy imaging

A

Common indications for radionuclide renal imaging with Lasix:

  • Suspected uretero-pelvic or uretero-vesical obstruction; pre and post-surgical evaluation
  • Hydronephrosis
  • Distension of pelvicalyceal system as an aetiology of back pain
21
Q

what are 5 non-medical, lifestyle treatment options offered for obstructive uropathy

A
  • Hydration
  • Quit smoking
  • Eat healthy / electrolyte balance / alcohol regulation
  • Regular exercise
  • Control hypertension
22
Q

what are 3medical management treatment options offered for obstructive uropathy

A
  • Secondary infection prevention (antibiotics)
  • Prophylactic antibiotics
  • Analgesics for pain
23
Q

what are 7 interventional management treatment options offered for obstructive uropathy

A
  • Drains
  • Surgery to repair anatomical defect
  • Ureteral stent
  • Nephrostomy tube (renal pelvis)
  • Ureteroscopic removal (stone)
  • Laser removal (stone)
  • Pyeloplasty (PUJ obstruction)
24
Q

what is renovascular hypertension?

A

The presence of systemic hypertension due to a stenotic or obstructive lesion within the renal artery

25
Q

what are 3 renovascular hypertension epidemiological facts?

A
  • Atherosclerotic lesions > 60% found in the kidney in 6.8% of population above age 65
  • Renal artery stenosis (RAS) found in 20% of patients with coronary disease
  • RAS found in 35% of patients with peripheral vascular disease
26
Q

what is the aetiology of renovascular hypertension

A
  • The most common and problematic cause is atherosclerotic renovascular disease
  • Atherosclerosis constitutes 84% of patients identified with renal artery stenosis
  • The two most common causes of RVH are:
    • Atherosclerotic renal artery stenosis (ARAS) = 90%
    • Fibromuscular dysplasia (FMD) = 10%
    • Possible for injury, tumour and clots
27
Q

what is the pathophysiology of renovascular hypertension?

A
  1. stenosis in the renal artery
  2. this causes an increase in renin and increased secretion of angiotensin II
  3. this results in vasoconstriction as well as aldosterone being released from the adrenal cortex
  4. aldosterone increases the blood volume
  5. increased blood volume and vasoconstriction leads to hypertension
28
Q

what are some signs and symptoms of renovascular hypertension

A
  • High blood pressure
  • Headache
  • Fatigue
  • Nausea and vomiting
  • Chest pain
  • Vision problems, confusion, anxiety
  • Excessive perspiration, pale or reddened skin
  • Sudden pain in the side
  • Bloody urine or clot in urine
  • sometimes no symptoms at all
29
Q

what are 3 clinical presentations of hypertension

A
  • abrupt onset/ sudden worsening of well-controlled hypertension
  • refractory to medical treatment with more than 3 drugs
  • age and sex (young women suggestive of FMD; older men suggestive of ARAS)
  • malignant or accelerated hypertension
  • no fam history of essential hyertension
30
Q

what are 3 clinical presentation of renal problems

A
  • azotemia induced or worsened by antihypertensive medications: ACE inhibitors or ARBs
  • unexplained azotemia
  • discrepancy in kidney sizes by more than 1.5cm with cortical scanning
  • bilateral small kidneys with cortical scanning
  • low-grade proteinuria with bland urinary sediment
31
Q

clinical presentation of other associated findings related to renovascular hypertension

A
  • laboratory evidence of persistent RAAS activation i.e. chronic hypokalemia
  • abdominal or flank bruit or both on physical examination
  • unexplained CHF symptoms or ‘flash’ pulmonary oedema
  • evidence of systemic atherosclerotic vascular disease i.e. CAD
  • smoking
  • severe retinopathy
  • left ventricular hypertrophy
32
Q

what are some laboratory markers used to diagnose renovascular hypertension

A
  • Tests to eliminate other renal disease:
    • Serum creatinine levels assess renal function
    • 24-hour urine collection for proteinuria
    • Urinalysis to eliminate RBCs in urine
    • Serologic tests for systemic lupus erythematosus or vasculitis
    -Peripheral renin may be elevated (but also in essential hypertension and ischaemic nephropathy)
    -Renin levels pre and post captopril
33
Q

what imaging modalities are utilised when imaging for renovascular hypertension

A
angiography/ arteriography
doppler US
CTA
MRA
scintigraphy
34
Q

when is angiography/ arteriography used for imaging renovascular hypertension and what are the advantages and disadvantages?

A

-Gold standard
-Invasive
-Radiation dose
-Risk of contrast-induced nephropathy
-Not used routinely unless
• Concurrent therapy with angioplasty, +/- stent
-The quality of images with DSA is not as good as with conventional angiogram

35
Q

when is doppler ultrasound used for imaging renovascular hypertension and what are the advantages and disadvantages?

A
  • Direct visualisation of the renal vascular tree
  • Assess blood flow velocity and pressure wave forms
  • Inter-operator variability
  • Useful when positive
  • Looking for major flow accelerations in a renal artery
36
Q

when is CTA used for imaging renovascular hypertension and what are the advantages and disadvantages?

A
  • 3D reconstruction of the vascular tree
  • Excellent sensitivity and specificity to see RAS
  • RAS anatomy
  • Potentially nephrotoxic
  • Radiation dose
37
Q

when is scintigraohy used for imaging renovascular hypertension and what are the advantages and disadvantages?

A

-Captopril-enhanced
-Non-invasive
-Assess functional status
-? bilateral RAS
-Not great in significant renal insufficiency
-Functional, not anatomical, diagnosis of RAS
-No direct visualisation of the renal arteries
-Interpretation, changes from baseline after ACEI:
• 10% change in cortical uptake
• 15% increase in cortical retention
• 2min+ increase in time to peak
• 2min+ delay in visulaisation of collecting system
-Curve that:
• Change in differential function
• Delayed time to peak
• Flattening of the curve
• Delayed clearance

38
Q

when is MRA used for imaging renovascular hypertension and what are the advantages and disadvantages?

A
  • Non-invasive
  • Excellent visualisation of the renal vasculature
  • Gadolinium contrast
  • High cost
  • Potential for nephrogenic systemic fibrosis for those with renal insufficiency
39
Q

what are some lifestyle changes used as treatment options for renovascular hypertension

A
• Quit smoking 
• Eat healthy 
• Regular exercise 
• Weight control 
• Control hypertension, hyperlipidaemia, diabetes 
These are the same for atherosclerosis
40
Q

what are some medical management treatment options for renovascular hypertension

A

management of risk factors:

  • ACE inhibitor for BP (ramipril, lisinopril for example)
  • (or ARB) +/- diuretic
  • Beta blocker for cardiac workload / BP
  • Calcium channel blocker relieves symptoms
  • Aspirin or anti-platelets (clopidogrel) reduces CV risk
41
Q

what are some interventional treatment options for renovascular hypertension

A
  • Stent
  • Surgery (rarely needed)
    • Bypass
    • Renectomy