Give the pathogenesis of a UTI. How can some bacteria evade the immune system? How does a UTI cause renal damage?
• Urinary tract usually protected by regular flushing to remove organisms.
• Between flushing, bacteria can climb urethra
• Fimbriae allow the attachment to host epithelium
• Urease produced by some bacteria help against the urea in urine
• K antigens produced by some bacteria allows production of polysaccharide capsule that helps evade immune system
• Haemolysins break down Hb and can cause renal damage.
Give the clinical symptoms of an upper and lower UTI
• Lower UTI – frequency and dysuria (difficulty passing urine)
• Upper UTI – acute pyelonephritis (infection in kidneys)
• Septicaemia +/- shock
• Loin pain
What would turbidity in a MSU suggest?
Give 3 investigations one can do to diagnose a UTI
• MSU – Mid stream urine. Mid stream collected so it isn’t contaminated by skin flora.
• If delay in screening should store in fridge and with boric acid to prevent proliferation of bacteria.
• Urine culture
• Urine Dipsticks – Used to detect:
o Leucocyte esterase – WBCs in urine
o Nitrite – Some bacteria convert nitrates to nitrite
• Turbidity indicates UTI.
• Microscopy for WBCs and RBCs.
What is complicated and uncomplicated cystitis? How would you treat them?
• Complicated cystitis – Everyone else, need to culture urine.
• Uncomplicated cystitis – In healthy women of child bearing age, no need to culture urine
Uncomplicated cystitis – Trimethoprim 3 day course
Complicated cystitis (inflammation of bladder):
• Trimethoprim or nitrofurantoin 5 day course.
How would you treat pylonephritis?
co-amoxiclave 14 day course
What are the 3 main categories of direct action diuretics? Where does each act? How do they work? Give examples of each category
1) Loop diuretics – act on loop of henle by blocking the Na-K-2Cl cotransporter e.g. bumetanide
2) Thiazide diuretics – act on early distal tubule and block the Na-Cl cotransporter e.g. metolazone
3) K+ sparing diuretics – Act on late DT and CD to block the ENaC e.g. amiloride
All block the action of Na+ transporters and prevent water being reabsorbed into the tubule cell.
How do aldosterone antagonist diuretics work? Give an example drug
• Aldosterone acts on principal cells of late DT and CD to increase Na reabsorption
• Antagonists block this action and reduce Na reabsorption
• E.g. sprionolactone
How does a diuretic which modifies filtrate content work? Give an example drug.
• Osmolarity of filtrate is increased as molecule is freely filtered at glomerulus and not reabsorbed.
• This decreases water, Na+, and K+ reabsorption.
• E.g. mannitol
How does inhibiting carbonic anhydrase work as a diuretic?
• Carbonic anhydrase inhibitors act on PT
• Interferes with Na and HCO3 reabsorption
• E.g. acetazolamide
What type of diuretic would you use for a hypercalcaemia?
What type of diuretic would you use for glaucoma?
Carbonic anhydrase inhibitor
What type of diuretic would you use for cerebral oedema?
Which diuretics can lead to hyperkalaemia and how?
K+ sparing diuretics and aldosterone antagonists:
• Rate of K+ secretion dependent on sodium absorption into the cell which creates a negative potential for the positive K+ ion to leave into the lumen
• Results in hyperkalaemia
Which diuretics can lead to hypokalaemia and how?
Loop and thiazide diuretics:
• Block Na+ and H2O reabsorption in LoH or early DT
• Leads to increased Na+ and H2O delivery to late DT and CD
o Faster flow rate of filtrate in tubule lumen means K+ secreted in lumen is washed away faster, therefore a lower K+ concentration in lumen generates a favourable chemical gradient for K+ secretion --> Hypokalaemia
Diuretics also reduce ECF volume which activates the RAS system and results in aldosterone secretion --> increased Na absorption and K+ secretion --> hypokalaemia