Med Term 3 > Urinary 8 > Flashcards

Urinary 8 Flashcards

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1
Q

What is the definition of a UTI?

A

an infection of any part of the urinary tract usually caused by bacteria but rarely by other microorganisms such as fungi, viruses or parasites

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2
Q

What types of UTIs can one acquire?

A

Upper UTI
- an infection of the upper tract, the kidneys and the ureters

Lower UTI
- infection of the bladder

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3
Q

What is the difference between a lower and an upper UTI?

A

lower = bladder (cystitis)

upper = upper part of tract, kidneys, ureters

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4
Q

What can also be considered lower UTIs?

What is the term ‘lower UTI’ actually intended to mean?

A

urethritis and prostatitis

infection of the bladder with no clinical evidence of urethritis, prostatitis, epididymitis or orchitis

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5
Q

What is the difference between a complicated and an uncomplicated UTI?

A

COMPLICATED = UTI in people with an increased chance of complications
- pregnant women
- men
- people with anatomical or functional abnormalities of the urinary tract, indwelling catheters
- people with renal diseases
- people with immunocompromising diseases

UNCOMPLICATED = acute, sporadic or recurrent lower/upper UTI with none of the features above

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6
Q

In the features on the image, what would make a UTI complicated or uncomplicated?

A
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7
Q

List 4 impaired immune responses which would complicate a UTI.

A
  • diabetes mellitus
  • HIV/AIDS
  • cancer
  • chronic steroid use
  • immunosuppressive therapy
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8
Q

List 3 impairments of neural control which would make a UTI complicated.

A
  • stroke
  • MS
  • spinal cord injury
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9
Q

List 4 exposure risks which would make a UTI complicated.

A
  • urinary incontinence
  • obesity
  • frailty
  • frequent abx use
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10
Q

List 6 anatomical or functional abnormalities which would complicate a UTI, categorising them in ‘obstructive’, ‘renal’ and ‘procedural’.

A

obstructive
- BPH
- urinary retention
- genital prolapse
- obstructive uropathy e.g stones, tumours

renal
-polycystic kidney disease
- horseshoe kidney
- CKD
- AKI

procedural
- recent urological surgery or instrumentation

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11
Q

In regards to recurrent UTIs, what is the difference between relapse and reinfection?

A
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12
Q

What is a recurrent UTI defined as?

A
  • 2 or more in 6 months
  • 3 or more in one year

(due to either relapse or reinfection)

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13
Q

What is a catheter associated UTI?

A

symptomatic infection of bladder or kidney in a catheterised person - can be either urethral or suprapubic

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14
Q

What is asymptomatic bacteriuria?

A

the presence of significant bacteria in the urine, as a result of colonisation of the urinary tract, WITHOUT symptoms or signs of infection

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15
Q

What is the percentage of UTIs which occurs in females?

A

80%

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16
Q

Up to 1 of all women will acquire acute UTIs in their lifetime.

A

50%

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17
Q

Who are UTIs rare in?

A

rare in healthy men <50

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18
Q

Incidence of UTIs rise with what?

A

age

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19
Q

UTIs are the __2__ most common health care associated infections after __3__ infections.

A

second

RTI

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20
Q

What 3 factors are taken into account in regards to developing UTIs?

A
  • BACTERIAL ENTRY
  • HOST FACTORS
  • CHANGES TO FLORA
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21
Q
  1. Why are women more prone to UTIs compared to men?
  2. Name two healthcare related risk factors for UTI.
  3. How does sexual intercourse increase UTI risk?
  4. Which groups are at higher risk of UTIs due to impaired immunity?
A
  1. because women have a shorter urethra
  2. catheter use, healthcare-associated infections, previous urinary tract instrumentation/surgery
  3. facilitates bacterial entry into the urethra
  4. immunocompromisede patients
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22
Q

Name 2 structural causes of urinary obstruction that increase UTI risk.

A

urethral strictures

stones

tumours

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23
Q

How does BPH predispose to UTIs?

A

causes urinary obstruction -> incomplete bladder emptying -> stasis -> infection risk

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24
Q
  1. Why are pregnant women more prone to UTIs?
A

hormonal and anatomical changes cause urinary stasis and reflux

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25
What is vesicoureteric reflux and why does it increase UTI risk?
backflow of urine from bladder to ureters/kidneys = promotes infection
26
1. How do abx predispose to UTIs? 2. Why does diabetes increase the risk of UTIs?
1. they normal vaginal and gut flora, allowing uropathogens to overgrow 2. glucosuria and impaired immune response encourage bacterial growth
27
28
Why are post-menopausal women more prone to UTIs?
reduced oestrogen -> changes in vaginal flora -> loss of protective lactobacilli
29
What is the most common causative pathogen in UTIs? List other causative pathogens.
uropathogenic E.coli - klebsiella - proteus - enterococcus - staph saprophyticus (young women) - pseudomonas (catheterised/hospital)
30
What UTI pathogens are associated with young women and catheterised/hospital?
staph saprophyticus (young women) pseudomonas (catheterised)
31
List 3 host defences against UTIs and explain what they do.
1. UMBRELLA CELLS (specialised epithelial cells in the bladder) - they stretch as bladder fills - when they shed they carry away any microbes stuck to them = PHYSICAL REMOVAL 2. UROPLAKIN COATING (proteins on the bladder lining) - forms a protective surface - limits exposure of receptors that bacteria could otherwise bind to - fewer docking sites for pathogens like E.coli 3. URINE FLOW & OSMOTIC STRESS - regular urination flushes microbes out before they can settle - urine also has high osmolarity and sometimes antimicrobial properties, making it a harsh environment for bacteria
32
How do umbrella cells in the bladder help defend against UTIs?
they stretch and shed, carrying away microbes attached to their surface
33
What is the role of uroplakin in UTI defence?
it coats the bladder surface, limiting receptor exposure and reducing bacterial binding sites
34
How does urine flow prevent UTIs?
constant flushing removes bacteria before they can adhere
35
Besides flow, what property of urine helps limit bacterial survival?
osmotic stress (high osmolarity) creates an unfavourable environment for bacteria
36
Explain how uropathogenic E.coli (UPEC) - manage to overcome the body's defences.
1. ADHESION - UPEC use fimbriae (pili) and adhesins to stick to bladder cells - they bind to mannose residues on the urothelial surface - they use CATCH-BONDING = bond gets stronger instead of being away by urine flow = bacteria stays stuck even during urination 2. INVASION - once attached they invade urothelial cells - inside they form intracelullar bacterial communities = protects them from immune system and abx 3. ASCENDING SPREAD - from the bladder they can travel up the ureters to the kidneys = PYELONEPHRITIS
37
What structures allow UPEC to adhere to the bladder lining?
fimbriae and adhesins
38
Which adhesin on type 1 fimbriae binds to mannose on urethial surfaces?
firmH adhesin
39
What is “catch-bonding” and why is it important in UTI pathogenesis?
a mechanism where adhesion becomes stronger under urine flow, preventing bacteria from being flushed away
40
After adhesion, how do UPEC survive in the bladder?
they invade urothelial cells and form intracellular bacterial communities (IBCs)
41
How do UPEC spread from the bladder to the kidneys?
by ascending through the ureters
42
What are typical symptoms of lower UTIs? What are they caused by?
- dysuria = inflamed urethral/bladder mucosa - frequency = bladder lining irritation - urgency = inflamed bladder wall - new nocturia = reduced bladder capacity - suprapubic tenderness = cystitis - urine changes = from pus, blood, debris - haematuria = mucosal inflammation
43
What is the "urinary triad" of cystitis?
dysuria, frequency, urgency
44
What is suprapubic tenderness consistent with?
bladder inflammation
45
New nocturia is a symptom particularly important in which group of people?
older adults
46
What are the Red Flag symptoms of UTIs?
47
About 50% of women who present with the clinical features of cystitis do not have positive urine cultures. What is this called?
urethral syndrome
48
What is urethral syndrome? Possible explanations of this include what?
condition with lower urinary tract symptoms but no evidence of bacterial infection on culture - infection with low counts of bacteria - infection with fastidious organisms not detected on routine culture - STI e.g chlamydia - non-infective inflammation e.g chemical
49
What further questions would you ask?
1. RED FLAGS - any fever, shivers or felt generally unwell - any pain in your back or sides, just under ribs 2. BLOOD IN URINE 3. PREGNANCY STATUS 4. PAST INFECTIONS - any urine infections before? how were they treated 5. SEXUAL/GYNAE HISTORY - any unusual discharge, itching or new sexual partners 6. MEDICAL RISK FACTORS - any other health problems, like diabetes, kidney problems or are you on any regular medication
50
List 4 differential diagnoses.
lower UTI upper UTI STI/PID ectopic pregnancy urethritis urethral syndome
51
How you would manage this? (history, examination, investigations)
52
What are the key steps in the NICE diagnostic and management pathway for women under 65 with suspected UTI?
STEP 1 - SYMPTOM CHECK - rule out non-UTI causes or urinary symptoms (vaginal discharge, STIs, menopause change) STEP 2 - KEY DIAGNOSTIC SYMPTOMS - dysuria, new nocturia, cloudy urine - 2-3 symptoms = UTI LIKELY -> no dipstick - 1 symptom -> do dipstick - no key symptoms = look for other severe urinary symptoms e.g urgency, frequency-> maybe dipstick
53
What are the main markers on a urine dipstick?
NITRITES = bacteria with nitrate reductase (but not all species) LEUKOCYTE ESTERASE = indicates WBCs (inflammation/infection) RED CELLS = haematuria, may support UTI but non-specific
54
What are limitations of urine dipstick? What can they be caused by?
false negative - short bladder dwell time - non-nitrate-reducers false positives - contamination - non-UTI inflammation
55
When are urine dipsticks helpful and when should they be avoided?
helpful in younger women with atypical symptoms avoid for diagnosis in >65s and catheterised adults
56
When is it advised to send urine culture?
- pregnant - suspected pyelonephritis - men - children <16 years - recurrent UTI or failed abx tx - GU tract abnormality or renal impairment - catheter associated UTI - immunocompromised e.g diabetes or immunosuppression - older adults >65 if symptomatic and starting abx
57
What is the first choice of abx for UTIs?
nitrofurantoin if eGFR >45ml/min - 100mg modified-released x2 daily (or if unavailable 50mg x4 daily) for 3 days trimethoprim if low risk of resistance - 200mg twice a day for 3 days
58
What advice would you give a patient on self-care measures for symptom relief?
59
What should be considered? What should be excluded? What are the next steps? What must not be sent acutely?
male with LUTS + perineal pain -> consider prostatitis haematuria -> exclude malignancy next steps - history and exam incl DRE - MSU for culture, urine dip, STI screen if risk - treat if prostatitis suspected MUST NOT SEND PSA ACUTELY
60
List 4 differential diagnoses.
- acute prostatitis - lower UTI - urethritis (STI) - acute epididymo-orchitis - bladder/prostate cancer
61
What are the symptoms of acute prostatitis?
- symptom triad of UTI - urinary retention - systemic infection (fever) - pains: low back, suprapubic, perineal, sometimes rectal - pain on ejaculation - exquisitely tender, enlarged, boggy prostate on DRE
62
What kind of pains would one experience in acute prostatitis?
- low back - suprapubic - perineal - sometimes rectal - pain on ejaculation
63
What is the first line treatment for acute bacterial prostatitis?
ciprofloxacin 500mg BD or ofloxacin 200mg BD ALTERNATIVE: trimethoprim 200mg BD (if quinolones unsuitable) treat 14 days then review - extend to 28 days if needed
64
What's the likely diagnosis? What makes it the likely diagnosis?
acute pyelonephritis - sudden onset of systemic and urinary symptoms - classic triad: FEVER >38/RIGORS, FLANK OR COSTOVERTEBRAL ANGLE PAIN/TENDERNESS, NAUSEA/VOMITING
65
1. What is the classic triad of acute pyelonephritis? 2. What are other common features? 3. What is it often preceded by? 4. How may this present in older adults?
2. malaise, myalgia, flu-like illness 3. often preceded by UTI symptoms (dysuria, frequency) 4. ATYPICALLY = confusion, lethargy, hypothermia instead of fever
66
In regards to the management of pyelonephritis, when should you admit the patient?
67
In regards to the management of pyelonephritis, what investigations should be done?
- serology = U+Es, FBC, CRP - cultures = urine and blood
68
In regards to the management of pyelonephritis, what antibiotics should be prescribed and what supportive care could be done?
cefalexin 500mg TDS-QDS 7-10 days (PO if able, IV abx if severely unwell, step down after 48 hours - review micro results and tailor therapy) supportive care: - analgesia - hydration - safety-netting
69
When can you give IV abx instead of PO in pyelonephritis? What should be done?
if PO abx cannot be tolerated or if severely unwell - step down after 48 hours, review micro results and tailor therapy accordingly
70
What is the preferred PO abx choice in pyelonephritis? Which PO abx should be avoided in pregnancy?
cefalexin 500 mg TDS-QDS 7-10 days (safe in pregnancy) - trimethoprim - ciprofloxacin
71
Who is asymptomatic bacteriuria common in? Should it be treated or not? Why?
in elderly, diabetic, catheterised and institutionalised patients do NOT treat - no benefit + increases resistance and side effects
72
When should exceptions be made for asymptomatic bacteriuria?
pregnancy before invasive urology procedures
73
How are UTIs in pregnancy managed?
74
What is the risk of untreated UTIs in pregnancy?
- pyelonephritis - preterm labour - low birth weight - increased risk of perinatal mortality
75
What UTI antibiotic should be avoided in pregnancy? Which abx is safe?
trimethoprim (esp in first semester) and fluoroquinolones cefalexin
76
UTIs in men are always what?
COMPLICATED
77
In regards to UTIs in men, when should a urology referral be done?
if UTI is recurrent, atypical or haematuria present
78
Persistent haematuria in men warrants what?
2WW cancer referral
79
When would a male qualify for referral to the 2WW cancer pathway?
uti with persistent haematuria
80
Why did the junior doctor decide against administering cephalosporin?
due to cross-sensitivity between cephalosporin and penicillin allergy
81
What is the mechanism of action of trimethoprim?
it is an inhibitor of the enzyme dihydrofolate reductase (DHFR) inhibition of this enzyme prevents active thymidylate synthesis - blocks the biosynthesis of purines, hence blocks DNA replication and eventually causes microbial cell death
82
What is the main complication of lower UTI?
ascending infection leading to upper UTI (acute pyelonephritis)
83
List all that the results show.
84
A patient has a UTI and is prescribed ciprofloxacin, 2 days later he is confused and his symptoms have worsened - he is diagnosed with pyelonephritis and started on IV meropenem. Three days later, the patient develops diarrhoea. What do you think the most likely cause of this patient's diarrhoea may be? If this is confirmed, what would be the most appropriate management of this patient?
antibiotic associated diarrhoea - c.diff in most cases ideally, abx should be stopped but this patient needs minimum of two weeks abx for pyelonephritis - CIPRO from GP more likely to cause diarrhoea than MEROPENEM STOP CIPRO, CONT MERO, START METRO 400MG TDS
85
A patient has a UTI and is prescribed ciprofloxacin, 2 days later he is confused and his symptoms have worsened - he is diagnosed with pyelonephritis and started on IV meropenem. 3 weeks later, his condition has improved and he is discharged. 3 months later, he presents to his GP again with symptoms of a UTI. What is the best choice of abx? (he was on cipro and IV mero, got diarrhoea, stopped cipro and started on metro during his last hospital stay)
86
In what situations may prophylactic antibiotics use be indicated? Give some disadvantages of the use of prophylactic antibiotics.
recurrent UTIs where the underlying cause cannot be corrected development of resistance, side effects e.g CDT diarrhoea, allergy and cost
87
Suggest possible reasons as to why Doris' condition hasn't improved with trimethoprim.
Doris may potentially be resistant to trimethoprim - potential poor drug compliance due to confusion could also be a factor - it is also possible that Doris isn't absorbing the drug due to vomiting
88
What is the commonest cause of UTIs? What bacterium is primarily involved?
faecal contamination of the urethra - E.coli
89
While at A&E, Doris becomes increasingly unwell and develops severe renal angle tenderness with swinging pyrexia and rigors. What does this set of symptoms imply about her UTI?
suggest UTI has ascended and has become acute pyelonephritis
90
1. How much dietary calcium do you eat per day? 2. From that, how much is absorbed through the gut and how much is secreted back? What is the net absorption? 3. How much comes out in faeces?
1. 1000mg 2. 300mg absorbed through gut, 100mg secreted back - net absorption = 200mg/a day 3. 800mg
91
What is the normal calcium concentration in ECF? What does it exist as?
2.2-2.5 mmol/L - ionised (active) calcium - protein-bound calcium
92
How much calcium to kidneys excrete into the urine?
about 200mg/day
93
How are bones and calcium linked?
bones = giant calcium store bones exchange calcium with blood: - quick buffering - slow exchange = deposition/reabsorption over long time
94
How much calcium is stored in bones?
1,000,000mg of calcium in 1kg of bone
95
1. Calcium is regulated through what? 2. What acts to increase plasma calcium? 3. What acts to increase whole body calcium? 4. What acts to decrease plasma calcium?
1. hormonal control 2. PTH 3. vit d metabolites 5. calcitonin
96
1. What does PTH do? 2. What does Vit D metabolites do? 3. What does calcitonin do?
1. acts to increase plasma calcium 2. acts to increase whole body calcium 3. acts to decrease plasma calcium
97
What is the physiological response to falling calcium levels?
1. parathyroid glands detect blood calcium is too low 2. parathyroid glands release PTH 3. PTH works in three main places to bring calcium back up: - BONE: stimulates bone resorption -> osteoclasts break down and release calcium into blood - KIDNEYS: ->increases calcium reabsorption = keeps more Ca2+ in blood, less lost in urine ->decreases phosphate reabsorption (phosphate would otherwise bind to calcium and reduce levels) ->stimulates calcitriol (active vit D) synthesis - INTESTINE: indirectly increases intestinal calcium absorption because calcitriol (from the kidney) helps the gut absorb more calcium 4. NEGATIVE FEEDBACK = calcium levels in plasma rise back to normal = PTH secretion falls
98
1. Which glands detect falling plasma calcium? 2. Which hormone is secreted in response to low calcium? 3. What effect does this hormone have on bone?
1. parathyroid glands 2. PTH 3. increases bone resorption, releasing calcium into blood
99
What effect does PTH have on the kidneys?
-increase calcium reabsorption = keeps more Ca2+ in blood, less lost in urine - decrease phosphate reabsorption = phosphate would bind calcium and reduce free levels - stimulate calcitriol (vit d) synthesis
100
1. How does PTH indirectly increase intestinal calcium absorption? 2. What type of feedback controls PTH secretion?
1. by stimulating calcitriol (active vit D) production in the kidneys 2. negative feedback - rising calcium levels inhibit further PTH release
101
How is vitamin D produced (introduced to the body) and activated in the body (to calcitriol)?
SKIN (UV light) + DIET - 7-dehydrocholesterol (a cholesterol precursor) is converted by UV-B light into cholecalciferol (vitamin D3) - oily fish, eggs, fortified foods LIVER - vitamin D3 is hydroxylated by 25-HYDROXYLASE in the liver = produces CALCIDIOL (25-HYDROXY-VITAMIN D) KIDNEY - CALCIDIOL further hydroxylated by 1-A-HYDROXYLASE (enzyme is stimulated by PTH) product = CALCITRIOL / 1,25-DIHYDROXY-VITAMIN D = ACTIVE FORM
102
Fill in the gaps.
103
What precursor in the skin is converted to vitamin D3 by UV-B light?
7-dehydrocholesterol
104
What is another source of Vitamin D3 apart from the skin?
dietary intake (oily fish, eggs, meat, fortified foods)
105
In which organ is vitamin D3 first hydroxylated and by which enzyme? What is the product of this?
liver - by 25-hydroxylase calcidiol (25-hydroxy-vitamin D)
106
In which organ is calcidiol converted to the active form of Vitamin D? By which enzyme? What is the active form of vitamin D called?
kidney - 1-a hydroxylase (stimulated by PTH) calcitriol / 1,25-dihydroxy-vitamin D
107
What does calcitriol bind to? What is the major effect of calcitriol? What is the minor effects of calcitriol?
binds to vit d receptor (a nuclear receptor) increased intestinal absorption of calcium and phosphate increased reabsorption calcium and phosphate and facilitates resorption of calcium
108
What does calcium normally do in neurons? What happens in hypocalcaemia?
calcium normally stabilises sodium channels in neurons in hypocalcaemia sodium channels become more permeable = nerves and muscles are easier to excite = THEY FIRE ACTION POTENTIAL MORE READILY = leads to the classic signs of hypocalcaemia
109
What happens to sodium channels in hypocalcaemia?
they become more permeable - nerves and muscles are easier to excite and they fire action potentials more readily
110
What are the symptoms of hypocalcaemia and why do you get them?
neuromuscular instability (tetany) - paraesthesia - muscle twitching - seizures - laryngospasm cardiac - prolonged QT interval - hypotension - arrhythmia
111
What are the signs of hypocalcaemia?
CHOVSTEK'S SIGN - twitching of the muscle of facial expression when the facial nerve is tapped TROUSSEAU'S SIGN - spasm of the hand and forearm when blood pressure cuff is inflated around the arm
112
What is Chovstek's sign? What is Trousseau's sign? What do they both indicate?
twitching of the muscle of the facial expression when the facial nerve is tapped spasm of the hand and forearm when a blood pressure cuff is inflated around the arm hypocalcaemia
113
What cardiac symptoms would a person with hypocalcaemia experience?
prolonged QT interval hypotension arrhythmia
114
What are the causes of hypocalcaemia? What are the treaments?
hypoparathyroidism - after thyroid surgery, autoimmune vit d deficiency - dietary deficiency, lack of sun exposure, CKD treatment - vit D/calcium supplementation - careful monitoring during thyroid surgery
115
How does the body respond to hypercalcaemia? (what detects rising calcium levels, what is secreted, what does that do - major and minor effect)
C CELLS (PARAFOLLICULAR cells) of thyroid sense high calcium they secrete calcitonin which does the following: 1. BONE (major effect) - inhibits osteoclast activity = stops bone resorption so less calcium released into blood 2. KIDNEYS (minor effect) - calcitonin decreases reabsorption of calcium and phosphate = more calcium and phosphate are lost in urine PLASMA CALCIUM LEVELS FALL BACK TOWARD NORMAL
116
What are the symptoms of hypercalcaemia? List 5.
-bone pain - renal stones -abdominal pain/nausea/vomiting - polyuria - confusion, altered behaviour, fatigue, coma
117
What are causes of hypercalcaemia (what are the two most common causes)? What is the treatment?
118
Where is most of the calcium reabsorbed in the nephron? How does this happen? Where is the rest reabsorbed?
PCT - 65% = happens paracellularly down an electro chemical gradient TAL - 25% DCT and CNT - 8%
119
What is happening here?
120
What is occurring here?
121
How is phosphate handled by the kidney?
122
List the 2 hormones that increase serum calcium. List the 1 hormone that decreases serum calcium.
123
What are the words for: 1. stones in the renal tract 2. stones in the kidney 3. pain experience with renal stones
1. urolithiasis 2. nephrolithiasis 3. renal colic
124
What is the meaning of the following: 1. urolithiasis 2. nephrolithiasis
1. stones in the renal tract 2. stones in the kidney
125
Where are renal stones most commonly found?
3 natural points of narrowing of the ureter: - pelvo-ureteric junction - at pelvic brim (where ureters cross iliac vessels) - vesico-ureteric junction
126
What is the basic mechanism for the formation of renal stones? List the 5 different types of renal stones and their colours.
crystals in supersaturated urine ADHERE to the UROTHELIUM, providing a 'NIDUS' for stone growth
127
What are the urinary and dietary factors as to why calcium stones form? Why do uric acid, struvite and cystine stones form?
128
What general factors contribute to the formation of stones? What is the epidemiology of renal tract stones?
dehydration personal history family history structural abnormality e.g horseshoe kidney COMMON male 3: female 1
129
What are clinical features of renal tract stones?
130
Why do people with renal tract stones experience renal colic?
131
What are the complications of renal tract stones? Which one requires urgent drainage?
132
In regards to complications of renal tract stones, obstruction and infection (static urine in kidney is infection) requires what?
urgent drainage
133
Which investigations are appropriate for renal tract stones?
134
What is the acute management of renal stones?
135
What is the surgical management for renal stones?
136
What treatment is used for smaller renal stones? Where is this performed?
137
What is a ureteroscopy? What is a percutaneous nephrolithotomy?
Med Term 3
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