Urinary Session 7 Flashcards

1
Q

What can cause obstruction of the renal tract and increase the risk of developing a UTI?

A
BPH
Pregnancy
Uterine prolapse
Stones
Tumours
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2
Q

What is commonly seen as a cause of ascending infection in children with UTIs?

A

Ureteric reflux

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3
Q

What is ureteric reflux?

A

Abnormal or dysfunctional bladder valves, particularly seen in children

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4
Q

How should all children with a UTI be investigated?

A

Ultrasound

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5
Q

Which valves are likely to be involved in males and females with ureteric reflux?

A

Males: posterior urethral
Females: vesico-ureteric

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6
Q

What are bacterial factors which increase the likelihood of developing a UTI?

A

Fimbriae
K-antigen
Urease
Haemolysins

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7
Q

How does K-antigen allow a bacterium to cause a UTI?

A

Allows production of a polysaccharide capsule

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8
Q

How do haemolysins aid in the pathogenesis of UTI?

A

Damage host cell membranes and cause renal damage

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9
Q

Which two bacterial factors do G-ve UTI causative agents utilise to cause infection?

A

K-antigen

Haemolysins

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10
Q

What are coliforms?

A

G-ve, non spore forming bacilli that can ferment lactose

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11
Q

How do the majority of UTIs develop?

A

Transmission of coliforms across the perineum

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12
Q

What is secreted in between episodes of bladder voiding in order to reduce the risk of UTI?

A

Antibacterial secretions

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13
Q

After coliforms, what is a common causative agent of UTI in young women and hospitalised pts?

A

Coagulase -ve staph

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14
Q

What demonstrates irritation of the bladder in lower UTI?

A

Frequency and dysuria +/- low grade fever and urgency with a typical burning sensation

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15
Q

How does acute polynephritis present?

A

Fever, loin pain or pain in renal angle +/- dysuria and frequency

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16
Q

How can bacteraemia lead to acute polynephritis?

A

Becomes localised by filtration in the glomerular tuft

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17
Q

When is asymptomatic UTI significant and why?

A

In the mother during pregnancy –> premature birth

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18
Q

Can UTI progress to septicaemia +/- shock?

A

Yes, large cause of G-ve septicaemia in secondary care

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19
Q

Who fits into the uncomplicated UTI group?

A

Healthy women of child-bearing age

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20
Q

How are UTIs diagnosed in the uncomplicated UTI group?

A

Clinical diagnosis + dipstick

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21
Q

Who fits into the complicated UTI group?

A

Females of non-child bearing age
Males
Pregnant females
Pts who have failed to respond to UTI Tx

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22
Q

How are UTIs diagnosed in the complicated UTI group?

A

Dipstick and culture

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23
Q

What host factors promote the development of a UTI?

A

Shorter urethra in females
Obstruction
Neurological problems
Ureteric reflux

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24
Q

How can urine specimens be collected in diagnosis of UTI?

A
Mid stream urine (MSU)
Clean catch (children)
Collection bags
Catheter sample
Supra-pubic aspiration
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25
Why do MSU samples have to be taken mid-stream?
So the first void can wash out flora
26
How are urine samples transported to the lab and why are these methods used?
@ 4 degrees Celsius to represent having just left bladder | +/- boric acid to preserve and restrict multiplication so a falsely raised pathogen count is not detected
27
What causes turbidity of urine to change in UTI?
WBC response to pathogen
28
Is using turbidity if urine to identify UTIs a good investigation to use?
Yes, it has high sensitivity so will identify +vex if you know there is an infection somewhere but you don't know where
29
What is measured in dipstick testing?
Leucocyte esterase Nitrite Haematuria Proteinuria
30
What do high levels of nitrite on a urine dipstick indicate?
Bacterial metabolism of urea
31
Which components of the urine dipstick test are good indicators for infection but do not specify the reason for WBCs in the urine?
Leucocyte esterase | Nitrite
32
Why do the haematuria and proteinuria components of a urine dipstick have low specifity?
There are a range of causes for both
33
When will microscopy be used to examine a urine sample?
Kidney disease Suspected endocarditis Children
34
What is examined during microscopy of a urine sample?
WBCs RBCs Bacteria Casts
35
What are seen on microscopy of contaminated urine samples?
Squames
36
What is carried out if microscopy of a urine sample is +ve?
Culture
37
What can cause a non-significant culture following a +ve microscopy investigation for UTI?
``` Abx treatment for another infection e.g. URTI Urethritis Vaginal infection TB Appendicitis ```
38
59% of adult women with a UTI have urethral syndrome. What can cause this?
``` Low count bacteriuria Fastidious organisms Vaginal infection/inflammation STIs --> urethritis Mechanical/physical/chemical e.g. Soaps ```
39
Why are only symptomatic catheterised pts treated for UTI?
They will always have a level of bacteriuria
40
What is the treatment for an uncomplicated UTI?
3-day trimethoprim/nitrofurantoin
41
What is the treatment for a complicated UTI?
7-day trimethoprim/nitrofurantoin with follow up for clearance of S/S and bacteriuria
42
What is the treatment for pyelonephritis and septicaemia due to UTI?
14-day ciprofloxacin/cefuroxime of IV gentamicin if necessary
43
What prophylactic treatment can be used for pts who experience 3 or more episodes of UTI per year?
Single nightly dose of trimethoprim/nitrofurantoin
44
Why is amoxicillin not used to treat complicated UTI?
Has 50% resistance
45
What general management strategies can be used for all UTIs?
Ensure voiding mechanism is correctly functioning | Stay hydrated
46
What is diuresis?
Increased formation of urine by the kidney
47
What is the symptom of diuresis?
Polyuria= >3l per day urine output
48
What is a diuretic?
A substance/drug that promotes a diuresis by increasing renal excretion of water and sodium (increased fraction excretion) and thus reducing ECF volume
49
What do diuretics that block sodium reabsorption by acting on ENaC also decrease?
K+ secretion
50
How can diuretics have a direct action on cells in the nephron?
Via secretion into the lumen of PCT --> flow downstream and directly bind to transporters
51
How do aldosterone antagonists work as diuretics?
Competitively inhibit aldosterone action therefore decrease ENaC sodium reabsorption and K+ sparing
52
How do osmotic diuretics work?
Modify filtrate content so small molecules are filtered by not reabsorbed and hence increase the osmolarity of filtrate
53
Are osmotic diuretics currently used clinically?
No
54
How does inhibiting carbonic anhydrase act as a diuretic?
Prevents CA activity on brush border of PCT therefore altering Na+ and HCO3- reabsorption
55
Are carbonic anhydrase inhibitors currently used clinically as diuretics?
No
56
Which drugs can be classified as K+ sparing diuretics?
Inhibitors of renal sodium channels - Amiloride | Aldosterone antagonists - Spironolactone
57
Why are loop diuretics very potent diuretics?
25-30% of filtered Na+ is reabsorbed in the loop of Henle and segments distal to this have limited capacity to reabsorb sodium resultant increase in sodium and water
58
Which diuretics act on the filtration barrier?
Osmotic diuretics
59
Which diuretics act on the PCT?
CA inhibitors
60
Where in the loop of Henle do loop diuretics act?
Thick ascending limb
61
What does the efficacy of CA inhibitors for diuresis in the PCT depend on?
HCO3- filtration, a lower lumen +ve potential causes decreased cation reabsorption
62
Where do thiazides act on the nephron to cause diuresis?
Distal tubule
63
What ion movements do thiazides cause?
Increases sodium loss and increases calcium reabsorption
64
Where do potassium sparing diuretics act in the nephron?
Collecting duct
65
Why are loop diuretics used to treat heart failure?
Due to diuretic, vaso- and venodilation effects to decrease after and preload
66
When are loop diuretics used to treat fluid retention and oedema?
In nephrotic syndrome, renal failure and cirrhosis of the liver if Spironolactone is not sufficient
67
How are loop diuretics used in the management of hypercalcaemia?
Furosemide and IV fluids are given to prevent dehydration
68
What is the clinical application of thiazide diuretics?
Used to treat hypertension due to vasodilation effects
69
Why are thiazide diuretics not used in renal failure?
Lack potency
70
What is a possible side effect of thiazide treatment?
Erectile dysfunction
71
What are the clinical applications of aldosterone antagonists?
Primary hyperaldosteronism Ascites and oedema in cirrhosis Survival benefit in chronic heart failure Additional Tx for hypertension not controlled by ACEI, CCB and thiazide
72
What is the clinical application of ENaC blockers?
Used with loop diuretics/thiazide to minimise potassium loss
73
What is the clinical application of CA inhibitors?
Used in glaucoma to decrease aqueous humour in the eye
74
What is a possible side effect of carbonic anhydrase inhibitors?
Can cause metabolic acidosis due to decreased HCO3-
75
What is the clinical application of osmotic diuretics?
IV mannitol in cerebral oedema to increase plasma osmolarity
76
What is the pathogensis of nephrotic syndrome which leads to a condition requiring diuretic Tx?
Glomerular disease --> increase in GbM permeability --> proteins lost in urine --> decreased plasma albumin which liver cannot compensate --> decreased plasma p(oncotic) --> peripheral oedema --> decreased circulating volume --> RAAS stimulation --> ECF expansion
77
How does cirrhosis of the liver lead to a condition requiring diuretic Tx?
Decreased albumin synthesis --> RAAS stimulation --> ECF expansion Portal hypertension --> increased p(venous) in GI --> decreased an p(oncotic) --> transudation from peritoneal capillaries to cavity --> ascites
78
Why is Spironolactone Tx preferred for cirrhosis of the liver?
Does not cause hypokalaemia
79
Why can Spironolactone Tx lead to gynaecomastia?
Oestrogen-like molecule
80
How are the different adverse effects of diuretics monitored?
K+ disturbances - monitor electrolytes Hypovolaemia - monitor weight and postural BP Hyponatraemia - monitor electrolytes
81
What are the possible adverse effects shared by loop and thiazide diuretics?
Increased uric acid levels due to competition of transporters --> gout Glucose intolerance due to insulin release interference Raised LDL levels
82
How can cirrhosis of the liver lead to hepatic encephalopathy?
Liver cannot detoxify ammonia --> increased levels in blood
83
How does hepatic encephalopathy present?
Constructional apraxia (can't draw a star) --> flapping tremors --> confusion --> coma
84
What creates a favourable lumen -ve potential for passive K+ secretion in the DCT and CD?
Rate of sodium reabsorption
85
How can loop and thiazide diuretics cause hypokalaemia?
Block sodium and water reabsorption in loop/early DT --> increased delivery to distal parts --> faster washing away of secreted K+ and increased reabsorption of sodium by principal cells creating favourable gradient --> more K+ in urine
86
How does the effect of diuretics on the RAAS lead to hypokalaemia?
Decrease ECF --> RAAS activation --> increased aldosterone --> increased sodium reabsorption and K+ secretion
87
How can diuretics lead to hyperkalaemia?
Aldosterone antagonists decrease activity of Na-K-ATPase and ENaC --> less sodium reabsorption --> less K+ secretion ENaC inhibitors cause less sodium reabsorption --> less K+ secretion
88
What management strategies can be used to when choosing diuretics to minimise K+ changes whilst maintaining diuretic action?
Loop/thiazide with K+ sparing diuretic | Loop/thiazide with K+ supplement
89
What other substances not used for Tx have diuretic action?
Alcohol Coffee Lithium Demeclocycline
90
How does alcohol act as a diuretic?
Inhibits ADH release
91
How does coffee act as a diuretic?
Increases GFR --> decreases tubular sodium reabsorption
92
How do lithium and demeclocycline act as diuretics?
Inhibit ADH action on CD
93
Which substances with diuretic action but are not Tx have pure water effects by changing osmolarity, not volume?
Alcohol | Lithium
94
Explain how some named diseases can cause diuresis.
DM: glucose in filtrate --> osmotic diuresis DI (cranial): decreased ADH release --> high pure water loss DI (neohrogenic): poor CD ADH repsonse --> high pure water loss Psychogenic polysdipsia: high fluid intake
95
Give an example of each type of diuretic with the following mechanism of action: direct action on cells, aldosterone antagonists, osmotic diuretics, CA inhibitor.
Bendroflumethiazide Spironolactone Mannitol Acetazolamide