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Urinary > Week 7 - UTIs and Diuretics > Flashcards

Week 7 - UTIs and Diuretics Flashcards

1
Q

Describe the pathogenesis of UTIs

A
  • Normal urinary tract is protected from infection by a variety of defence mechanisms
    — Regular flushing during voiding, which removes organisms from the distal urethra
    — Between voiding, these organisms may ascend the urethra
  • Commonest pathogens = gram-negative rods
    — Particularly enterobactericeae (coliforms, especially E.coli)
    — Coagulase-negative staphylococci cause infections in young women and in hospitalised patients
  • Host factors:
    — Shorter urethra (more infections in females)
    — Obstruction (enlarged prostate, pregnancy, stones, tumours)
    — Neurological problems (incomplete emptying, residual urine)
    — Ureteric reflux (ascending infection from bladder, especially in children)
  • Bacterial factors:
    — Adhesion
    • Fimbriae and adhesins allow attachment to urethral and bladder epithelium
    — K antigen permits production of polysaccharide capsule
    • Provides defence and protection
    — Urease
    • Produced by some bacteria
    • Breaks down urea creating a favourable environment for bacterial growth
    — Haemolysins
    • Damage host membranes and cause renal damage
    — Faecal flora
    • Potential urinary pathogens colonise periurethral area
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2
Q

What are the symptoms of bacterial cystitis?

A

Frequency and dysuria, often with pyuria and haematuria

- Lower urinary tract infection

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3
Q

What are the symptoms of abacterial cystitis?

A

Frequency, dysuria, pyuria, haematuria but no significant bacteriuria
- Lower urinary tract infection

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4
Q

What are the symptoms of prostatitis?

A

Fever, dysuria, frequency with perineal and low back pain

- Lower urinary tract infection

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5
Q

What are the symptoms of acute pyelonephritis?

A

Symptoms of cystitis plus fever and loin pain

  • Cystitis symptoms: Frequency and dysuria, often with pyuria and haematuria
  • Upper urinary tract infection
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6
Q

What are the symptoms of chronic interstitial nephritis?

A

Renal impairment following chronic inflammation

- Upper urinary tract infection

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7
Q

What are the symptoms of covert bacteriuria?

A

Asymptomatic

  • Detected only by culture
  • Important in children and pregnancy
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8
Q

How can you investigate for diagnosis of a UTI?

A
  • Dipstick tests are available for the detection of:
    — Blood
    — Leukocyte esterase (indicating white blood cells)
    — Nitrite (indicating the presence of nitrate-reducing bacteria)
  • Turbidity
  • May include microscopy for:
    — WBCs
    — RBCs
    — Squamous epithelial cells
  • The number of bacterial colonies cultured from urine specimens is estimated to give a bacterial count
    — Significant bacteria: > 105 colony forming units of a single organism per ml of urine
    — Interpretation of culture results depends on:
    • Clinical details (symptoms, previous antibiotics)
    • Nature and quality of specimen
    • Delay in culture
    • Species isolated
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9
Q

When would you require repeat urine specimens?

A
  • Low bacterial counts
  • Evidence of contamination
  • ‘Sterile pyuria’ – WBCs in the urine without bacterial growth, may be caused by:
  • – Prior antibiotic
  • – Urethritis (Chlamydia or gonococci)
  • – Vaginal infection or inflammation
  • – Fastidious organisms
  • – Non-infective inflammation (e.g. tumours, chemicals)
  • – Urinary tuberculosis
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10
Q

How can you test for an uncomplicated UTI?

A

Infection indicated by nitrite/leucocyte esterase dipstick testing
- No culture needed

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11
Q

How can you test for an complicated UTI?

A

Culture

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12
Q

How do you treat an uncomplicated UTI?

A
  • A short (typically 3 day) course of an oral antibacterial agent
  • – E.g. trimethoprim or nitrofurantoi
  • Increased fluid intake
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13
Q

How do you treat a complicated UTI?

A
  • 7 day course
  • Trimethoprim, nitrofurantoin or cephalexin may be used
  • – Amoxicillin is NOT appropriate because 50% of isolates are resistant
  • Increased fluid intake
  • Address underlying disorders
  • Post-treatment follow-up culture
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14
Q

When is a UTI complicated?

A

If patient is:

  • Pregnant
  • Male
  • Underlying disorders
  • Child
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15
Q

How do you treat acute pyelonephritis?

A
  • Treatment, initially systemic, for 10-14 days
  • Possibly IV initially
  • May use ciprofloxacin, cefuroxime, gentamicin (IV only)
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16
Q

How do you treat a UTI in catheterised patients?

A
  • Antimicrobial treatment is usually only recommended in patients with systemic features
  • Catheter should be removed if possible
17
Q

When would you give prophylaxis for a UTI?

A
  • 3 or more episodes in 1 year
  • No treatable underlying condition
    Give: single nightly dose of trimethoprim or nitrofurantoin
18
Q

Describe the use of loop diuretics

A
  • Block Na-K-2CL transporter
  • Secreted into the lumen of the PCT
  • Travel downstream to act at the loop of Henle
  • Very potent diuretics
  • Have a diuretic effect, as well as vaso- and venodilatory effects
  • Used to treat fluid retention and oedema in:
  • – Nephrotic syndrome
  • – Renal failure
  • – Cirrhosis of the liver
  • Useful in treatment of hypercalcaemia
19
Q

Describe the use of carbonic anhydrase inhibitors

A
  • Not particularly potent
  • Acts on the PCT
  • Inhibit NaHCO3- reabsorption
  • – As it inhibits carbonic anhydrase in brush border and PCT cell
  • – There is less HCO3- in the glomerular filtrate so there is a reduced effect on Na+ ion reabsorption
  • Increase excretion of HCO3- with accompanying Na+, K+ and water
  • – Results in an increased flow of an alkaline urine and metabolic acidosis
  • Plasma [HCO3-] declines during chronic use of these drugs because of the increased urinary excretion of HCO3-
  • Not used as diuretics anymore, but used in the treatment of glaucoma
20
Q

Describe the use of thiazide diuretics

A
  • Block Na-Cl cotransporter in DCT
  • – Increases Na+ loss in urine
  • Secreted into lumen in PCT
  • Travel downstream to act at DCT
  • Reduces Ca2+ loss in urine
  • Less potent than loop diuretics
  • Ineffective in renal failure
  • Widely used in hypertension
  • Higher incidence of hyperkalaemia
21
Q

Describe the use of K+ sparing diuretics

A
  • Inhibitors of epithelial (ENaC) channels
    — Mild diuretics
    — Usually used in combination with K+ losing diuretics to minimise K+ loss
    • Such as loop of thiazide diuretics
  • Aldosterone antagonists
    — Best drug for treatment of hypertension due to primary hyperaldosteronism
    — Preferred drug for ascites and oedema in cirrhosis
    — Used in addition to loop diuretics in heart failure
  • Both groups:
    — Reduce the loss of K+
    — Reduce Na+ channel activity
    — Are mild diuretics
    — Can produce life-threatening hyperkalaemia
    — Don’t use with K+ supplements
    — Only use with normal renal function
22
Q

Describe osmotic diuretics

A
  • Small inert molecules
  • Increases plasma osmolarity thus drawing out fluid from tissues and cells
  • Freely filtered in the kidney but not reabsorbed, so increases the osmolarity of the filtrate
  • Acts by altering the driving force for renal water absorption, which is osmolarity
23
Q

How can loop and thiazide diuretics cause hypokalaemia?

A

Increased Na+ and H2O delivery to late DCT and CD causes:

  • Faster flow rate of filtrate in tubule lumen
  • – K+ secreted into lumen is washed away faster
  • – Lower [K+] in lumen, so favourable chemical gradient for K+ secretion
  • – Hence more K+ loss in the urine
  • Increased Na+ absorption by principal cells
  • – Favourable electrical gradient for K+ excretion
  • – Hence more K+ loss in the urine
24
Q

How can diuretics cause hyperkalaemia?

A

May occur with K+ sparing diuretics

  • Reduced activity of ENaC and Na-K-ATPase reduces Na+ absorption
  • Hence reduces potassium loss in urine
25
Q

What are some adverse effects of diuretics?

A
  • Potassium abnormalities
  • Hypovalemia
    — Especially loop diuretics
    — Excessive loss of Na+ and water
    — Monitor:
    • Weight
    • Blood pressure
    • For signs of dehydration
  • Hyponatraemia
  • Increased uric levels in the blood
    — With thiazide and loop diuretics
    — Can precipitate attack of gout
  • Erectile dysfunction
    — Thiazide diuretics
26
Q

What other substances can cause diuresis?

A
  • Alcohol: inhibits ADH release
  • Coffee: increases GFR and decreases tubular Na+ reabsorption
  • Other drugs: lithium, demeclocycline
  • – Inhibit ADH action on collecting ducts
27
Q

What are some diseases that cause diuresis?

A
  • Diabetes mellitus
  • – Glucose in filtrate, so osmotic diuresis
  • Diabetes insipidus (cranial)
  • – Decreased ADH release from posterior pituitary
  • Diabetes insipidus (nephrogenic)
  • – Poor response of collecting ducts to ADH
  • Psychogenic polydipsia
  • – Increased intake of fluid
28
Q

What can diuretics be used to treat?

A
  • Hypercalcaemia
  • – Loop diuretics promote calcium excretion in the loop of henle
  • Hypertension
  • – Thiazide diuretics
  • – Spironolactone
  • – Resistant hypertension
  • Acute pulmonary oedema
  • – IV furosemide
  • Kidney failure
  • – Unable to excrete Na+ and H2O
  • – Need loop diuretics
  • Conditions with ECF expansion and oedema
  • – Congestive heart failure
  • – Nephrotic syndrome
  • – Cirrhosis with ascites and oedema
29
Q

How does congestive heart failure cause ECF expansion and oedema?

A
  • Increased systemic venous pressure leads to oedema
  • – Fluid moves from intravascular to interstitial compartment
  • Drop in cardiac output with reduced renal perfusion
  • Leads to activation of RAAS
  • – Na+ retention causes expansion of ECF
30
Q

How does nephrotic syndrome cause ECF expansion and oedema?

A
  • Glomerular disease that leads to increased glomerular basement membrane permeability to protein
  • Proteins are filtered and lost in urine, causing:
  • – Low plasma albumin which results in low plasma oncotic pressure and hence peripheral oedema
  • Reduced circulatory volume
  • RAAS activated
  • Na+ and water retention
  • Expansion of ECF and more oedema
31
Q

How does cirrhosis cause ECF expansion and oedema?

A
  • Reduced albumin synthesis in liver
  • – Causes low plasma albumin which results in low plasma oncotic pressure and hence peripheral oedema
  • Portal hypertension
  • – Causes increased venous pressure in splanchnic circulation
  • – High venous pressure and low oncotic pressure
  • – Movement of fluid from peritoneal capillaries to peritoneal cavity (transudate)
  • – Ascites (fluid in peritoneal cavity)
  • Oedema and ascites lead to reduced circulatory volume:
  • – RAAS activated
  • – Na+ and water retention
  • – Expansion of ECF and worsening oedema and ascites

Urinary (10 decks)

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