Session 7 - UTI and DIuretics Flashcards
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
- Fever
- Loin pain
What would turbidity in a MSU suggest?
UTI
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 Haematuria
o Proteinuria
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?
Loop diuretic
What type of diuretic would you use for glaucoma?
Carbonic anhydrase inhibitor
What type of diuretic would you use for cerebral oedema?
Osmotic diuretic
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
