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Clinical Conditions > 9. Urinary > Flashcards

9. Urinary Flashcards

1
Q

What is renal agenesis?

A

Lack of development of kidney, causes symptoms if bilateral.

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2
Q

What causes renal agenesis?

A

Failure of the ureteric bud to interact with the metanephric blastema and stimulate the future metanephros to grow.

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3
Q

What is Wilm’s tumour?

A

Congenital malignant tumour of the metanephric blastema in otherwise well chidlren.

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4
Q

What is a duplication defect?

A

Ureteric bud splits before it stimulates metanephros so there is an extra kidney or the kidney divides into two lobes.

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5
Q

What is a common sequelae of a duplication defect?

A

The extra kidney or lobe gives rise to an ectopic ureteric orifice.

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6
Q

What is a horseshoe kidney?

A

Fusion of the kidneys in the midline by their inferior poles during ascent which causes them to get caught on the inferior mesenteric arteries in ascent.

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7
Q

Where do horseshoe kidneys sit?

A

Just inferior to the inferior mesenteric artery.

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8
Q

What is an ectopic ureteric orifice?

A

The ureter opens into somewhere other than the trigone of the bladder, causing incontinence and chronic inflammation of epithelia at new opening as they’re not used to urine content.

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9
Q

What is cystic kidney disease?

A

Multicystic leading to atresia of the ureter, or polycystic which is incompatible with life.

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10
Q

How is cystic kidney disease detected?

A

Oligohydramnios during foetal development.

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11
Q

What causes urorectal fistulae?

A

Usually a defect in the urogenital sinus leading to a failure of cloacal portioning so there is communication between urinary and GI tracts.

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12
Q

What are the results of urorectal fistulae?

A

Infection due to colonic flora and irritation due to urea content.

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13
Q

What is exstrophy of the bladder?

A

A result of incomplete obliteration of the allantois/urachus so the bladder opens onto the abdominal wall and there is leakage of the urine through the umbilicus - incontinence.

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14
Q

What is ectopic urethral orifice?

A

Urethra opens into somewhere other than the correct place on the external genitalia - incontinence.

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15
Q

What is hypospadia?

A

Defect in the union of urethral folds in males so there is a urethra opening onto the ventral surface of the penis rather than at the end of the glans.

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16
Q

How does renovascular disease cause hypertension?

A

Renal artery stenosis or aneurysm leads to a reduced perfusion pressure in the kidney. This is detected by macula densa cells so there is more renin release and ATII created so hypertension.

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17
Q

What is diabetes insipidus?

A

Creation of large amount of dilute urine due to either a lack of production of ADH (neurogenic) or insensitivity to ADH (nephrogenic).

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18
Q

What are the consequences of diabetes insipidus?

A

Dangerous dehydration.

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19
Q

How is diabetes insipidus treated?

A

ADH injections of nasal spray.

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20
Q

What is syndrome of inappropriate ADH productions (SIADH)?

A

Huge overactivity of ADH production from a pituitary adenoma so there is excessive fluid retention and dilutional hyponatraemia.

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21
Q

How is SIADH managed?

A

Remove the source of hyponatraemia which otherwise leads to systemic cell lysis and death.

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22
Q

What is hypercalcaemia defined as?

A

[Ca2+] > 2.5mmol/L.

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23
Q

What are the common causes of hypercalcaemia?

A

Haematological malignancies, non-haematological malignancies, primary hyperparathyroidism, vitamin D toxicity.

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24
Q

What are the symptoms of hypercalcaemia?

A

Stones, depression, anorexia, nausea/vomiting, constipation, bone pain, hypertension, shorted QT interval on ECG.

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25
Q

What is the treatment for hypercalcaemia?

A

Hydration, furosemide - loop diuretic, bisphosphonates (protect bones), IV calcitonin, treat underlying condition.

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26
Q

What are renal calculi?

A

Stone within the collecting system of the urinary tract, normally calcium stone - urine saturated with calcium and oxalic acid so forms calcium oxalate that precipitates as a stone.

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27
Q

What are the three most common sites for stones in the urinary system?

A

Ureteropelvic junction (as ureter begins at renal pelvis), ureteric crossing of iliac vessels/pelvic brim, ureterovesical junction (where ureter ends at the bladder).

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28
Q

What are the symptoms of renal calculi?

A

Haematuria, renal colic - rolling around on floor in pain, post-renal AKI if it obstructs both kidneys, symptoms of pyelonephritis if infection from stasis, nausea, increased frequency and urgency of urinating.

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29
Q

What are the investigations for renal calculi?

A

Bloods to check PO4(3-), PTH, and Ca2+ levels. Abdominal X ray to spot radio-opaque stones (Ca2+ oxalate), ultrasound scan, non-constrast CT if negative AXR.

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30
Q

How are renal calculi managed?

A 
Small stones (<4mm) passed naturally, increase fluid intake and decrease Na+/oxalate intake.
Large stones (>6mm): extracorporeal shockwave lithotripsy (ESWL) - uses vibration to obliterate stone, non invasive; ureteroscopy; open surgery - very rare.
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31
Q

What is hyperkalaemia defined as?

A

[K+] > 5mmol/L.

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32
Q

What are the causes of hyperkalaemia?

A

External balance dysfunction: increased intake; decreased excretion.
Internal balance dysfunction: DKA (no insulin); cell lysis; metabolic acidosis.

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33
Q

What are the symptoms of hyperkalaemia?

A

Heart ECG changes: tented T waves, prolonged PR interval, ST depression, QRS widening, VF, asystole.
GI: paralytic ileus.
Acidosis: K+ uptake into cells promotes H+ movement into ECF.

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34
Q

How is hyperkalaemia acutely managed?

A

IV calcium gluconate to protect heart, move K+ into ECF using insulin and dextrose, remove K+ by dialysis as last resort.

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35
Q

How is hyperkalaemia managed long term?

A

Change diuretics, treat diabetic ketoacidosis, reduce dietary intake, gut resins to bind K+ to inhibit dietary uptake.

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36
Q

What is hypokalaemia defined as?

A

[K+] < 3.5mmol/L.

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37
Q

What are the causes of hypokalaemia?

A

External balance dysfunction: excessive GI loss (diarrhoea and vomiting), renal loss (loop diuretics).
Internal balance dysfunction: metabolic alkalosis from vomiting.

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38
Q

What are the symptoms of hypokalaemia?

A

Heart ECG changes: hyperexcitability from hyperpolarisation, low/absent T wave (no pot, no tea - no potassium, no T waves).
GI: paralytic ileus.
Skeletal muscle: muscle weakness.
Renal: unresponsive to ADH so nephrogenic diabetes insipidus.

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39
Q

What is the acute management of hypokalaemia?

A

Treat cause, replace K+ - dietary or IV, spironolactone/ACE inhibitors with excessive mineralocorticoid activity.

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40
Q

What are urinary tract infections?

A

Colonisation of the urinary tract with bacteria.

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41
Q

What are the types of urinary tract infection?

A

Simple/uncomplication (cystitis) - woman of reproductive age, most common.
Complicated (cystitis) - men, children, uncommon.
Pyelonephritis (upper) - inflammation of renal pelvis, can cause kidney injury, or septic shock.
Chronic nephritis.

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42
Q

What are the influencing host factors of UTIs?

A

Gender - females have shorter urethras and shorter distance between perianal area and bladder.
Obstruction of collecting system - benign prostatic hyperplasia, pregnancy, etc.
Neurological lesions - incomplete emptying with stasis.
Ureteric reflux - angle hasn’t changed before puberty so ascending bladder infection in children.
Comorbidites - diabetes, CKD, AKI, etc.

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43
Q

What are the influencing bacterial factors of UTIs?

A

Fimbrae - epithelial attachment.
Haemolysins - damaged host membranes for nutrition.
K antigens on polysaccharide capsule so evasion f macrophages.
Urease so NH3 production for bacterial growth.
E. coli fits all this.

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44
Q

What are the common causative pathogens of UTIs?

A

E. coli, enterobacteriacae, enterococci (atypical), staphylococci.

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45
Q

What are the symptoms of cystitis?

A

Frequent urination, pyuria (burning when weeing), bad smelling urine, cloudy urine, malaise.

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46
Q

What are the symptoms of pyelonephritis?

A

Fever and chills, nausea and vomiting, renal pain, SIRS if severe.

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47
Q

What are the investigations of UTIs?

A

Urine samples for cloudiness and dipstick test for nitrite/leukocyte esterase.
MCS of urine samples (for complicated, pyelonephritis, comorbidities) - WBC/RBC count, culture for pathogens.

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48
Q

How are UTIs treated?

A

Conservative: fluid intake; address comorbidites/underlying conditions.
Antibiotics: uncomplicated - 3 days of trimethoprim; complicated - 7 days of trimethoprim/nitrofurantoin; pyelonephritis - 14 days of ciprofloxacin/cefuroxime.
Recurrent: low dose trimethorpim/nitrofurantoin for prophylaxis.

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49
Q

What is stress urinary incontinence?

A

Involuntary passing of urine in response to exertion - coughing, sneezing.

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50
Q

What is the typical history with stress urinary incontinence?

A

Childbirth, previous pelvic surgery.

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51
Q

What are the examinations for stress and urge urinary incontinence?

A

Weight and height, abdominal exam, female - external genitalia stress test, male - prostate exam.

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52
Q

How are stress and urge urinary incontinence investigated?

A

Urine dipstick test, frequency and volume chart, bladder diary, pressure/flow studies.

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53
Q

How are stress and urge urinary incontinence treated generally and contained incontinence?

A

General: decrease fluid/caffeine intake, avoid constipation, stop smoking.
Contained incontinence: indwelling catheter, condom catheter, incontinence pads.

54
Q

What are the conservative, pharmacological, and surgical treatments for stress urinary incontinence?

A

Conservative: pelvic floor exercises.
Pharmacological: dulotexine (increases external urethral sphincter activity in filling phase).
Surgical: females - low tension vaginal tapes to support mid urethra, retropubic suspension procedure to correct position of bladder neck, intramural bulking agents to increase urethral wall size; males - artificial urethral sphincter with control in scrotum so artificial continence.

55
Q

What is urge urinary incontinence?

A

Urinary incontinence preceded or accompanied by urgency.

56
Q

What are the conservative, pharmacological, and surgical treatment for stress urinary incontinence?

A

Conservative: voiding scale training - void every hour and hold or leak in between, increase time by 15 mins a week until 2-3 hour is reached.
Pharmacological: cholinergic antagonists (oxybutynin) to block M3 receptors so detrusor relaxes and less urge to void, B3 agonists (mirabegron) to stimulate B3 adrenoceptors so detrusor relaxes, botunlinum toxin to block ACh release at M3 receptors so loss of detrusor contraction.
Surgical: sarcal nerve neuromodulation, augmentation cystoplasty (use bowel as bladder), urinary diversion (send to GI tract).

57
Q

What is acute kidney injury?

A

Clinical syndrome encompassing abrupt decline in GFR, increased [NH3] and [urea], acid/base disturbance, and Na+ upset.

58
Q

What are the stages of AKI?

A
  1. Serum creatinine >26.5mmol/L or >150% of patient’s baseline.
  2. SCr >200% of baseline.
  3. SCr >354mmol/L, acute rise of >44mmol/L in <24hours, >300% of baseline.
59
Q

What is the pre-renal acute kidney injury a result of generally?

A

Renal insult from hypoperfusion of the kidney, anything that causes decreased O2 delivery to >50% of the kidney parenchyma.

60
Q

What are the pre-renal causes of AKI?

A

Hypovolaemia, systemic vasodilation, left ventricular failure, renal artery aneurysm/stenosis/thrombus/emolus, impairment of renal autoregulation - preglomerular vasoconstriction from sepsis, posterglomerular vasodilation from ACE inhibitors.

61
Q

What is the pathophysiology of pre-renal AKI?

A

Decreased Na+ to macula densa from reduced GFR causes prostaglandin release to dilate afferent arteriole, and renin release causing efferent arteriole vasoconstriction.

62
Q

How can pre-renal AKI be treated?

A

With fluid resuscitation.

63
Q

What is acute tubular necrosis?

A

A result of decompensation following pre-renal AKI that sees the loss of function of the tubular cells.

64
Q

What are the implications of acute tubular necrosis?

A

Fluid flows through and out into the urine at a constant rate due to PCT cells damage, this means the kidneys can’t respond to changes in osmolarity so fluid resuscitation for pre-renal AKI treatment leads to hyponatraemia.

65
Q

What are the causes of acute tubular necrosis?

A

Ischaemia, nephrotoxins, rhabdomyolysis (huge breakdown of skeletal muscle causing high myoglobin release - nephrotoxin).

66
Q

What is intrinsic renal AKI?

A

Any pathological process that actually affects the renal parenchyma.

67
Q

What are the causes of intrinsic renal AKI?

A

Glomerular disease - inflammation clogs glomerulus so GFR declines.
Acute tubulo-interstitial glomerulonephritis - infection from pyelonephritis or toxin induced.
Haemolytic uraemic syndrome, malignant hypertension, pre-eclampsia damage endothelium so cause microvascular thrombi which occlude small arteries and decrease O2 to renal parenchyma.

68
Q

What is post-renal AKI?

A

Obstruction of the collecting tract causes increased intraluminal pressure so a backup and hydronephritis and renal impairment.

69
Q

What are the types of post-renal AKI?

A

Intraluminal - renal calculi, thrombus, tumour.
Within wall - post TB stricture.
Extrinsic - hyperplastic prostate, tumour, aneurysm.

70
Q

What does post-renal AKI cause?

A

Renal colic and haematuria.

71
Q

What is the presentation of AKI?

A

Elderly, hypotensive, nauseated, lethargic.

72
Q

What is the history of pre-renal AKI?

A

Hypovolaemic sock - tachycardia, hypotensive, peripheral cyanosis, decreased JVP.
Septic shock - tachycardia, hypotensive, red and warm peripheries, decreased capillary refill time, rigors, pyrexia.

73
Q

What is the history of intrinsic AKI?

A

Nephrotoxin drug history, UTIs, trauma.

74
Q

What is the history of post-renal AKI?

A

Renal colic (flank pain T11-L3), anuria, palpable bladder, potentially enlarged prostate.

75
Q

How is AKI investigated?

A

Urinalysis - nitrites, blood and protein (suggestive of intrinsic).
Urine biochemistry - pre-renal causes high urine osmolarity and low Na+, ATN causes low urine osmolarity and high Na+.
Serum biochemistry - urea and creatinine high for all, hypocalcaemia, hyponatraemia, hyperkalaemia.
Imaging - ultrasound scan, chest X ray, abdominal X ray.
Renal biopsy - differentiates type of renal AKI when unsure.

76
Q

What is the management of pre-renal AKI?

A

Correct fluid balance and treat underlying insult.

77
Q

What is the management of acute tubular necrosis?

A

Supportive of normal body homeostasis.

78
Q

What is the management of intrinsic AKI?

A

Supportive of normal body homeostasis, treat specific causes.

79
Q

What is the management of post-renal AKI?

A

Remove the blockage.

80
Q

When is dialysis used for AKI?

A

Persistent hyperkalaemia despite treatment, fluid overload despite treatment, metabolic acidosis where NaHCO3- is contraindicated, dialysable nephrotoxin, severe uraemia.

81
Q

What is nephrotic syndrome?

A

> 3.5g of protein lost in urination in <24hours.

82
Q

What are the causes of nephrotic syndrome?

A

Minimal change glomerulonephritis - podocyte damage seen under transmission electron microscopy.
Focal segmental glomerulosclerosis - scarring in isolated areas of glomerulus that leads to filtration dysfunction.
Membranous glomerulonephritis - immune deposits in sub-epithelial space so leaky membrane.

83
Q

What is the result of membranous glomerulonephritis?

A

1/3 get better, 1/3 show no change, 1/3 progress to renal failure.

84
Q

What is nephritic syndrome?

A

Damage to glomerulus so significant haematuria with proteinuria and decreased renal function.

85
Q

What are the causes of nephritic syndrome?

A

IgA nephropathy - most common, mesangial proliferation and scarring with IgA deposits.
Thin GBM nephropathy - hereditary benign nephropathy, thin GBM leads to isolated haematuria.
Alport syndrome - X linked recessive abnormal collagen IV so dysfunction of basement membrane.
Goodpasture syndrome - anti-GBM disease, overnight onset of severe nephritic syndrome from antibody to collagen IV.
Vasculitis - systemic inflammation of blood vessels from attack of ANCA and neutrophils, segmental necrosis.

86
Q

How is goodpasture syndrome treated?

A

Immunosuppression and IgG plasmophoresis if quick enough.

87
Q

What are the risk factors for prostate cancer?

A

Increased age, black>white>asian, family history - BRCA2 gene.

88
Q

Why isn’t prostate cancer screened for?

A

Doesn’t increase quality or length of life and prostate specific antigen isn’t specific to prostate cancer.

89
Q

What is the presentation of prostate cancer?

A

Elderly, haematuria, renal colic, asymptomatic, bone bain if metastasised.

90
Q

How is prostate cancer investigated?

A

Rectal exam, PSA blood test, bone scan, tranrectal ultrasound biopsy.

91
Q

How is prostate cancer treated?

A

If localised - surveillance, radial prostatectomy or radiotherapy.
If advanced localised - surveillance, hormones, or radiotherapy.
If metastasised - surgical/medical castration with LHRH agonists to slow growth, bisphosphonates protect bone, chemotherapy, and radiotherapy.

92
Q

What are the risk factor for bladder cancer?

A

Smoking, schistosomiasis, occupational exposure to carcinogens.

93
Q

How is bladder cancer staged?

A

TNM stages. T stages:
T1 = up to submucosa.
T2 = penetrated <50% thickness of detrusor.
T3a = penetrates 50-100% thickness of detrusor.
T3b-T4b = penetrated entire thickness of detrusor.

94
Q

How is bladder cancer treated?

A

Depends on type.
Non-muscle invasive - surveillance and intravesical chemotherapy.
Muscle invasive - neoadjuvant chemo/radiotherapy along with reconstructive surgery: ileal conduit; orthotopic reconstruction use bowel as bladder.

95
Q

What is renal cell carcinoma?

A

Cancer of the kidney parenchyma.

96
Q

What are the risk factors for renal cell carcinoma?

A

Smoking, obesity, dialysis.

97
Q

What are the common metastases of renal cell carcinoma?

A

Perinephric spread to secondary renal tumours.
Lymphatic spread to nodal metastases.
Venous drainage to IVC obstruction and tumour clot.

98
Q

What is the treatment for renal cell carcinoma?

A

Surveillance, radical nephrectomy. Palliative - molecular angiogenesis antagonists, sunitinib.

99
Q

What is upper tract transitional cell carcinoma?

A

Cancer from the kidney down to the trigone.

100
Q

What are the risk factors of upper tract transitional carcinoma?

A

Smoking, phenacetin - a now discontinued pain killer, Balkan’s nephropathy (familial interstitial nephritis).

101
Q

What is the treatment for upper tract transitional carcinoma?

A

Radical removal of kidney, fat, ureter, and part of the trigone.

102
Q

What is chronic kidney disease?

A

Irreversible and progressive degeneration in renal function over months to years. Replacement of renal parenchyma with fibrous scar tissue leading to shrunken, fibrotic kidney that’s not specialised for function.

103
Q

How is CKD classified into stages?

A

GFR base: G1 - >90ml/min to G5 - <15ml/min = renal failure.
ACR (albumin:creatinine ratio): A1 <3 to A3 >30.
Combine scores for a code, e.g. G3aA3.

104
Q

What are the causes of CKD?

A

Diabetes, hypertension, renal artery sclerosis, infection, genetics, obstruction/reflux nephropathy, idiopathic.

105
Q

What is the presentation of CKD?

A

CV - atherosclerotic plaques form, hypertension etc.
Ca2+ regulation - loss of Ca2+ in filtrate and more H3PO4-. Osteomalacia, osteititis fibrosa cystica, renal osteodystrophy.
Bodily pH - acidosis from inability to retain HCO3-.
Anaemia - from decreased secretion/sensitivity to EPO so less RBC productoin.
Breathlessness, seizure, aches and pains, nausea and vomiting, itching.

106
Q

How is renal function measured?

A

Inulin clearance - true GFR.

eGFR - creatinine levels and then adjust for age, gender, and if black.

107
Q

How is the cause of chronic kidney disease established?

A

Context from past medical history. Blood tests for immunoglobulin (IgA nephropathy), ANCA (vasculitis/lupus), CRP (infection), etc. Imaging for pathology: USS (hydronephrosis secondary to obstruction), CT (renal artery stenosis/aneurysm), MRI (renal artery stenosis/aneurysm).

108
Q

What are the treatments for chronic kidney disease?

A

Modify lifestyle factors - smoking, obesity, lack of exercise. Treat comorbidities - diabetes and hypertension. Treat underlying pathology. Reduce lipid intake and amount (statins). ACE inhibitors if proteinuria. Dialysis or renal transplant if end stages.

109
Q

What is end stage renal disease?

A

Level of renal function that would cause death without intervention, GFR <15ml/min generally.

110
Q

What are the symptoms of end stage renal disease?

A

Tiredness/fatigue/difficulty sleeping/difficulty concentrating. Volume overload as can’t excrete fluid. Anaemia. Bone disease. Acidosis. Uraemic symptoms. Increased sensitivity and narrowing of therapeutic index of many drugs due to decreased metabolism and or excretion.

111
Q

What are the types of renal replacement therapy?

A

Haemodialysis, peritoneal dialysis, kidney transplant.

112
Q

Describe the process of haemodialysis.

A

Creates an arteriovenous fistula that can be used to allow a point for withdrawal of 300mls of blood at a time. Exchange along an extracorporeal circuit that causes diffusion between sterile dialysis fluid and blood across a semi permeable membrane so toxins are eliminated. Heparin is given to prevent clotting.

113
Q

What are the advantages to haemodialysis?

A

Less responsibility for own care, get 4 days off a week from treatment, good evidence for long term effectiveness.

114
Q

What are the disadvantages of haemodialysis?

A

Arteriovenous fistula can be a cosmetic problem, limits travel and holidays as have to keep specific appointment, can damage CVS due to volume change.

115
Q

What are the contraindications of haemodialysis?

A

Failed vascular access, heart failure, coagulopathy.

116
Q

Describe the process of peritoneal dialysis.

A

Uses the peritoneum as the semi-permeable membrane. Peritoneum is filled with dialysis fluid and the exchange with the ECF/blood vessels allows for toxin elimination. One type has 4-5 bag changes a day, the other has overnight bags.

117
Q

What are the advantages of peritoneal dialysis?

A

Autonomy of care, less fluid/diet/travel restriction than haemodialysis.

118
Q

What are the disadvantages of peritoneal dialysis?

A

No days off, frequent changes, responsibility, indwelling catheter increases risk of peritonitis and hernias etc.

119
Q

What are the contraindications of peritoneal dialysis?

A

Failure of peritoneum, patient/carer can’t connect bag, obese/dench.

120
Q

Describe the process of kidney transplants.

A

Gold standard for renal replacement therapy. Kidney is implanted in at the iliac fossa instead of normal T11-L2 so the iliac vessels and bladder can be easily accessed.

121
Q

What are the types of kidney donor?

A

Deceased after brain death, deceased after circulatory death, live donation (related or altruistic).

122
Q

What are the advantages of kidney transplants?

A

Restores renal function to a much higher level than dialysis, no repetitive treatment, lower mortality than dialysis, good long term prognosis.

123
Q

What are the disadvantages of kidney transplants?

A

Risk of operative mortality, limited donor supply, life long immunosuppression so infection more likely, not a permanent fix.

124
Q

What are the advantages of peritoneal dialysis?

A

Autonomy of care, less fluid/diet/travel restriction than haemodialysis.

125
Q

What are the disadvantages of peritoneal dialysis?

A

No days off, frequent changes, responsibility, indwelling catheter increases risk of peritonitis and hernias etc.

126
Q

What are the contraindications of peritoneal dialysis?

A

Failure of peritoneum, patient/carer can’t connect bag, obese/dench.

127
Q

Describe the process of kidney transplants.

A

Gold standard for renal replacement therapy. Kidney is implanted in at the iliac fossa instead of normal T11-L2 so the iliac vessels and bladder can be easily accessed.

128
Q

What are the types of kidney donor?

A

Deceased after brain death, deceased after circulatory death, live donation (related or altruistic).

129
Q

What are the advantages of kidney transplants?

A

Restores renal function to a much higher level than dialysis, no repetitive treatment, lower mortality than dialysis, good long term prognosis.

130
Q

What are the disadvantages of kidney transplants?

A

Risk of operative mortality, limited donor supply, life long immunosuppression so infection more likely, not a permanent fix.

Clinical Conditions (13 decks)

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