Urinary Symptoms

Urinary Symptoms

1. Diabetes Mellitus

   • Chronic complications:
     • Mechanism = Hyperglycaemia > Mitochondrial overproduction of superoxide (ROS) > not enough enzymes to break down excess glucose > activates 4 major pathways of hyperglycaemic damage by inhibiting GAPDH. These are the Polyol, Hexosamine, Protein kinase C, and AGE Pathways. Hyperglycaemia damages blood vessels.
     • Microvascular damage = Retinopathy, Nephropathy, Neuropathy
     • Macrovascular damage = Coronary artery disease eg. atherosclerosis Cerebrovascular disease Peripheral vascular disease
   • Acute complications:
     • DKA (usually T1DM)
     • HHS (usually T2DM)
     • Hyoglycaemia
   • Onset of Type I diabetes

2. HAEMATURIA - what it can suggest

   • Visible 'macroscopic'
     • Not haematuria (mimics)
       • Beetroot
       • Myoglobin
     • Visible = Urine colour
       • White wine + clots
         • Rosé
           • Red wine = many clots
             • Coca-cola = kidney pathology
     • Acute Kidney Injury AKI
       • eg. due to RHABDOMYOLYSIS > Muddy-brown casts (myoglobin clogging kidney tubules) & myoglobinuria.
         • NB. rhabdomyolysis - myoglobin contains HEME so reacts positively to dipstick. But may be no blood under microscopy.
     • Urinary tract KUB / Prostate cancer
       • *Painless haematuria in men is a red flag for cancer!
     • IgA nephropathy (due to HSP)
       • Henoch-Schonlein Purpura = small-vessel vasculitis. IgA deposits in vessels (kidney and skin) > glomerular nephropathy. Presents with vis/non-vis haematuria & palpable purpuric rash. Can cause sore throat (synpharyngitic haematuria) - tonsilitis activates IgA so more likely to stick in kidneys/skin
         • Ttment: drugs to lower protein in urine or immunosuppression (to reduce inflammation)
   • Non-visible NVH 'microscopic'
     • Symptomatic
       • Kidney stones 'Renal calculi'
     • Asymptomatic
       • ANCA vasculitis
         • Circulating antibody (ANCA) > SYSTEMIC VASCULITIS and GRANULOMATOSIS of multiple target organs. Causes pulmonary-renal syndrome = rapidly progressive kidney injury and lung injury eg. pulmonary haemorrhage
           • Ttment: immunosuppression (steroids/cyclophosphamide/rituximab) to stop ANCA production
         • Diagnosis: ANCA antibody positive and Renal biopsy shows FOCAL SEGMENTAL NECROTISING GN (glomerulonpehritis) with CRESCENT FORMATION
           • Diagnose EARLY! (as presents similar to viral illness)
     • NVH = Dipstick - tetramethylbenzidine reacts with HEME > oxidised chromogen (green-blue)
       • Blood+ and Protein+ = sign of GLOMERULAR problem
       • NVH = Microscopy - Looks at RBCs WBC, epithelial cells, any casts?
         • Dysmorphic/acanthocyte RBCs / RBC casts = GLOMERULAR problem
           • Abnormal is >3 RBCs/ HPF. BUT no RBCs on microscopy does not mean no blood. RBCs lyse on the way to the lab
     • False result
       • NVH present in 2.5% of population. Of these, <1.5% will have significant disease eg malignancy. SO in practice, dipstick is the definitive test for NVH - as risk of overinvestigating.
         • NVH = EITHER 2 positive urine dipsticks (out of 3 tests) OR >3 RBCs/HPF by microscopy

3. Oedema

   • Can be explained by forces in capillaries (generated by HYDROSTATIC PRESSURE vs PLASMA ONCOTIC PRESSURE)
     • Sample interstitial fluid protein content to work out cause
       • Other proteins can also be measured: lactate dehydrogenase; fluid/serum protein...
         • Transudate = low protein content: <30 g/l
         • Exudate = high protein content: >30 g/l
         • TYPES OF OEDEMA
           • Why can pulmonary oedema occur without changes in venous pressure?
       • NORMAL =
     • Problems
       • 1) If we INCREASE capillary hydrostatic pressure by INCREASING VENOUS PRESSURE: Filtration is more affected by changes in VENOUS pressure than in arterial pressure > OEDEMA
         • Caused by: LEFT HEART FAILURE > ^pressure in the pulmonary venous circulation
           • Pulmonary wedge pressure (PWP) INCREASES – estimate of pulmonary capillary/ venous pressures – is in the range 5-12 mm Hg. As PWP rises (18-25 mmHg) evidence of water forced out > PULMONARY OEDEMA
         • Caused by: HEART, LIVER, KIDNEY DISEASE / problems with localised veins / Pregnancy / DVT > ^pressure in the systemic venous circulation
           • > PITTING OEDEMA
         • TRANSUDATE
       • 2) If we DECREASE capillary oncotic pressure by REDUCING PROTEIN CONC IN THE BLOOD: Water moves out of the blood by osmosis > OEDEMA
         • Caused by: NEPHROTIC SYNDROME - Damage to the basement membrane of the glomerulus > PROTEINURIA (frothy) and HYPOALBUMINAEMIA
           • Oedema commonly around the eyes, puffy face and pitting oedema in feet and ankles
             • Caused by IMPAIRED PROTEIN SYNTHESIS:
               • Reduced protein INTAKE (kwashiorkor)
               • MALABSORPTION (pancreatic insufficiency, CF, Damage to intestine surface: coeliac/viral enteritis)
               • Impaired HEPATIC SYNTHESIS (liver, albumin, 69 kD protein)
         • TRANSUDATE
       • 3) If we INCREASE EXTRAVASCULAR oncotic pressure by INCREASING PROTEIN CONC IN INTERSTITIUM
         • Caused by: CAPILLARY LEAK SYNDROME in SEPSIS (usually bacterial - gram +/-) and DEEP BURNS (oedema continues after hours after burns occured)
         • EXUDATE

4. Polyuria & thirst

   • See Kidney Function & Control map for ADH, RAAS, ANP, Diabetes Insipidus
     • Kidney Function & Control

5. Drugs to ^ urine output

   • CATHETERS
     • Foley Catheter
       • = tube & balloon. Two ports at end - one to drain urine, one to inflate balloon with H2O.
     • 3-Way Foley Catheter
       • 3 lumens at distal end of catheter (first 2 normal, third allows irrigation of bladder with saline to prevent and remove clots). Used if pt has had bleeding from urinary tract > haematuria and clots (either pathologically or from surgery)
     • Intermittent Catheter
       • Only inserted temporarily to drain residual urine post-voiding. No balloon as do not remain in bladder. Pt’s often taught to self-catheterise at home.
     • Suprapubic Catheter
       • Inserted into suprapubic region of lower abdo wall (superior to pubic symphysis) into bladder using guidewire. Full bladder required so it extends beyond the true pelvis and the overlying peritoneum is displaced superiorly. Use if: a urethral catheter causes regular UTIs/there has been trauma to urethra/pelvic floor muscles/pt is sexually active/for comfort.
     • Watch Geeky Medics video of insertion
       • https://geekymedics.com/penile-catheterisation-osce-guide/
       • REASONS TO INSERT: Urinary retention, Haematuria, BPH/Prostate Cancer, Urinary incontinence/retention related to nerve damage, Critically unwell, Pre-op

6. Kidneys

   • Great video of anatomy&nbsp; Kidneys: https://aclandanatomy-com.bris.idm.oclc.org/MultimediaPlayer.aspx?multimediaId=10528651 Female: https://aclandanatomy-com.bris.idm.oclc.org/MultimediaPlayer.aspx?multimediaId=10528661 Male: https://aclandanatomy-com.bris.idm.oclc.org/MultimediaPlayer.aspx?multimediaId=10528655
   • (Nephrotoxicity) - Drugs to be careful of

7. Lower urinary tract symptoms LUTS

   • INCONTINENCE SYMPTOMS
     • stress, urgency, mixed, overflow, nocturnal enuresis, postural incontinence, continuous, insensible, coital incontinence
       • Risk increases with age. F>M. Stress incontinence common in women.
         • Not a BLADDER problem. Result of abdominal pressure^ squeezes bladder. Failure of outflow tract to maintain resistance against this.
     • post-micturition leakage
   • BLADDER STORAGE SYMPTOMS
     • OAB Overactive bladder - urgency, frequency, nocturia +/- incontinence
       • OAB risk increases with age. M<>F.
         • Ttment: antimuscarinics, β3 agonists, botulinim toxin
           • Nocturia ttment: Conservative methods (bladder retraining, lifestyle changes), Percutaneous tibial nerve stimulation (PTNS), short-acting diuretics (taken in day), Imipramine (in children), Desmopressin (DDAVP)
   • VOIDING SYMPTOMS
     • hesitancy, straining to void, slow +/- interrupted stream, splitting or spraying, terminal dribble, position-dependent micturition, incomplete emptying
       • Risk increases with age (particularly men). M>F.
         • Detrusor sphincter dyssynergia, Bladder Outflow Obstruction (BOO)
   • LUT innervation
     • Kidney Overview, Urinary Tract, Micturition/Continence
     • Revisit Micturition/Continence

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