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ESA 3 > Urinary 7 > Flashcards

Urinary 7 Flashcards

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1
Q

At what stages of life are UTIs more common?

A

Infancy/Preschool:

Males experience a rise in prevanelnce of UTI at 0-5 yrs

Females experience the same rise from ages 0-10

Mid life:

Women in the 20s experience a rise in UTI prevalence as sexual activity increases

UTIs due to sexual activity are known as ‘Honeymoon cystitis’

Later life:

From ages 60+ both sexes experience a rise in UTI prevalence

In men this is due to prostatism and a greater rise in prevalence is seen

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2
Q

What are some host factors affecting UTI?

A

Urethral length:

Shorter urethra in women raises risk of UTI

Obstruction:

Prostatism, pregnancy, stones and tumours can all increase risk of UTI

Neurological problems:

Incomplete emptying of the bladder and residual urine can increase UTI risk

Ureteric reflex:

Reflux of urine into the ureters increases UTI risk

Ascending infection from the bladder common in children

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3
Q

What are the common sites of urinary tract obstruction?

For each site, what is the likely cause(s) of obstruction?

A

Pelvic-ureteric junction:

Caliculi (stones)

Ureters:

Caliculi, retroperitoneal fibrosis

Bladder:

Neuropathic bladder

Vesico-ureteric junction:

Caliculi

Prostate:

Benign prostatic hypertrophy

Urethra:

Stricture

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4
Q

What are the virulence factors that increase a bacteria’s ability to cause UTI?

A

Fimbriae:

To allow attachment to host epithelium

K antigen:

Permits production of polysaccharide capsule

Haemolysins:

Damage membrane and cause renal damage/inflammation

Urease:

Breaks down urea creating a favourable evirnoment for bacterial growth

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5
Q

What are the common pathogens in UTI?

A

G- bacilli (Enterobactericae/Coliforms, E. coli)

Coagulase (-) staphylococci

Other G- (E.g. Pseudomonas aeruginosa)

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6
Q

How can we differntiate Upper UTI and Lower UTI clinically?

A

UUTI Symptoms/signs:

Fever

Loin pain

Maybe dysuria and increased frequency of urination

LUTI Symptoms/signs:

Sometimes low grade fever

Dysuria

Increased frequency of urination

Urgent need to urinate (w/ Little urine produced)

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7
Q

Give 3 Lower UTIs and their characterisitic

A

Bacterial cystitis:

Frequency and dysuria often with pyuria (WBCs in urine) and haematuria

Abacterial cystitis:

As above but without significant bacteriuria

Prostatism:

Fever, dysuria, frequency with perineal and low back pain

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8
Q

Give 2 forms of upper UTI and their characterisitics

A

Acute pyelonephritis:

Symptoms of cystitis (Frequency, dysuria, pyuria, haematuria)

+ Fever and Loin pain

Chronic interstitial nephritis:

Renal impairement following chronic inflammation, infection is one of many causes

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9
Q

What is Covert Bacteruria?

A

Bacteriuria only detected by culture

Significant in children and pregnancy

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10
Q

What is a common complication of UTI?

A

Common source of G-neg bacteriaemia and subsequent septicaemia +/- shock

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11
Q

When is a urine sample needed to confirm clinical diagnoses of UTI?

A

Not needed in uncomplicated UTI (healthy women of child bearing age)

Urine culture needed for complicated UTI such as:

    • Pregnant patient*
    • Treatment failure for UTI*
    • Reccurent infection*
    • Suspected pyelonephritis*
    • Complications*
    • Male or Paediatric*
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12
Q

What near bed testing and laboratory testing is available for diagnoses of UTI?

A

Near bed:

Turbidity inspection

Dipstick

Labratory:

Microscopy

Urine Culture

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13
Q

How might a urine sample be collected?

A

Mid stream urine sample:

Avoids contamination of bacteria in urethra or on skin by washing them away before sample collection

Clean catch (paediatric)

Collection bag:

20% false positives

Catheter sample

Suprapubic aspiration

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14
Q

How should a urine sample be handled?

A

Kept at 4 degrees

+/- boric acid as a bacteriostatic

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15
Q

Describe how visual inspection of a urine sample can aid in diagnosis of UTI

A

Turbid urine would indicate a high bacteria/cell count, likely indicating a UTI

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16
Q

What is tested for by a urine dipstick?

A

Leucocyte esterase:

Detects WBcs

Nitrite:

Indicates presence of nitrate reducing bacteria

Haematuria

Proteinuria

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17
Q

What is disptick testing used for and not used for?

A

Used for:

Children >3

Men with mild/non-specific symptoms

Elederly women

Not used for:

Uncomplicated UTI

Men with typical/severe symptoms

Catherterised patients (false positives)

Older patients with no features of infection (asymptomatic bacteriura common)

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18
Q

Why is urine microscopy useful for diagnosis of UTI?

A

Can identify RBCs and WBCs in urine indicating UTI

Can identify contaminated samples (Epithelial cells present)

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19
Q

What are the diagnostic criteria for significant bacteriuria?

Why is this significant?

A

>10^5cfu/ml distinguishes bacteriuria/contamination from healthy patients

A single positive specimen is 80% predictive of pyelonephritis

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20
Q

What is the role of cultures in UTI diagnosis?

A

Investigation of children, males and complicated cases

High sensitivity (10^2cfu/ml detected)

Identification of specific organism:

Epidemiology of isolates

Susceptibility data

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21
Q

How is bacterial susceptibility to antibiotics determined?

A

Agar diffusion test:

Different antibiotics will create larger or smaller zones of inhibition of bacteria

Antibiotic with largest zone of inhibition is best

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22
Q

What are the causes of abacterial cystitis?

A

Low count bacteriuria

Fastidious organisms

Vaginal infection/inflammation

Sexually transmitted pathogens - urethritis

Mechanical, physical and chemical causes of inflammation

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23
Q

When is imaging of the urethral tract used in UTI cases?

What are the structures of interest?

A

UTIs in children

Also, can identify renal involvement in septic patients

Structures:

Male = Posterior urethral valve (Bladder outlet obstruction)

Female = Vesico-ureteteric valve/junction (VU reflex)

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24
Q

What is sterile pyuria and what might be the cause?

A

Pyuria present without bacteriuria

Causes:

Previous antibiotic

Urethritis

Vaginal infection/inflammation

Fastidious organisms

Non-infective inflammation (tumours, chemicals)

Urinary TB

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25
Describe asymptomatic bacteriuria
High prevalence in older people (women) Generally with associated pyuria (Positive dipstick) Not associated with increase in mortality/morbidity Leads to unneccessary antibiotic treatment Only requires action in pregnancy and urology surgery
26
What are the general prinicples of UTI treatment?
Increase fluid intake Address underlying disorders 3 day antibiotic course of uncomplicated 5 days for complicated (paeds, pregnant, male, underlying disorder)
27
Outline the treatment of simple cystitis
Uncomplicated infection 3 day course of trimethoprim or nitrofurantoin
28
Outline treatment of complicated UTI
Trimethoprim, nitrofurantoin or cephalexin for 5 days Cultures during follow up
29
Outline the treatment of pyelonephritis/septicaemia
14 day antibiotic course Use systemic agent (Co-amoxiclav, Ciprofloxacin, Gentamicin) IV antibiotics if acutely unwell
30
Outline UTI prophylaxis When is it used and what is it?
**When:** 3 or more infections in one year No treatable underlying condition **What:** Trimethoprim or nitrofurantoin Single nightly dose All breakthrough infections documented
31
What is a diuretic? What are it's effects?
**Diuretic:** A drug/substance that promotes diuresis **Diuresis:** Increased urine formation by kidney **Effects:** Increase fractional excretion of sodium Hence increasing excretion of Na+ and Water Leads to a reduction in ECF volume
32
When are diuretics used?
In conditions where Na+ and water retention cause ECF expansion (E.g. Heart failure)
33
Outline the general mechanism for Na+ and water reabsorption from the nephron
Cells contain Basolateral Na+/K+ ATPase and Apical Na+ channels/transporters Na+/K+ ATPase creates Na+ gradient across apical membrane Luminal Na+ moves into the cell down conc gradient utilising a channel or transporter Water moves into the cell down the osmotic gradient created by Na+ reabsorption
34
Each tubule segments have differnt apical channels/transporters, list which are found in each segment
**PCT:** Na+/H+ antiporter Na+ - AA/Glucose symporters **LoH:** Na+/K+/2Cl symporter **Early DCT:** Na/Cl symporter **Late DCT and CD:** ENaC
35
Outline the mechanism of Na+ reabsorption and related processes by principal cells How can this process be modulated?
Basolateral Na+/K+ ATPase creates gradient across apical membrane Na+ enters via apical ENaC This creates a negative lumen potential, this favours K+ secretion through apical K+ channels **Aldosterone:** Increases expression of Na+/K+ ATPase, NEaC and K+ channels
36
Outline the classes of diuretics that work by direct action on luminal cells
**Loop diuretics:** Work on LoH Block Na+/K+/Cl symporter **Thiazide diuretics:** Act on Early DCT Block Na/Cl cotransporter **K+ sparing diuretics:** Act on late DCT and CD Block ENaC
37
How do diuretics that work via direct actions on cells exert their effects?
Secreted into the lumen in the PCT Act on cells from within lumen
38
Outline how diuretics that antagonise the action of aldosterone function
Aldosterone antagonists reduce expression od Na/K-ATPase, ENaC and K+ channels on principal cells This reduces Na+ absorption and K+ secretion
39
How do osmotic diuretics work?
Freely filtered at glomerulus Not reabsorbed, remaining in lumen Increased osmolarity of filtrate leads to reduced water and Na+ reabsorption throughout tubule
40
How do enzyme inhibitor diuretics typically work?
Acts on PCT Inhibition of carbonic anhydrase: *- Enzyme that catalyses H2O + CO2 HCO3- + H+* Interferes with Na+ and HCO3- reabsorption
41
Give the 6 groups that diuretics are classified into and give examples of each
**Loop diuretics:** Furosemide **Thiazide diuretics:** Bendroflumethiazide **K+ sparing diuretics:** Amiloride **Aldosterone antagonists:** Spironolactone **Carbonic anhydrase inhibitors:** Acetazolamide **Osmotic diuretics:** Mannitol
42
Describe why loop diuretics are so potent
**Very potent:** 20-30% Na+ reabsorbed in LoH Segments beyond have limited capacity to reabsorb large amounts of Na+ so a high % is lost
43
What are some uses of Loop diuretics?
**Heart failure:** Reduced ECF + vaso and venodilation **Acute pulmonary oedema:** furosemide given IV for rapid action **Fluid retention and oedema in:** Nephrotic syndrome Renal failure Cirrhosis **Hypercalcaemia:** Impairs Ca2+ absorption in LoH IV fluids must be given as well
44
Dscribe the potency of thiazide diuretics Give uses Give common side effects
**Potency:** Only inhibits 5% of Na+ reabsorption **Uses:** Hypertension (also cause vasodilation) **Side effects:** Higher incidence of hypokalaemia Increases Ca2+ absorption
45
What are the similarities between K+ sparing diuretics and Aldosterone antagonists?
Both are mild diuretics (2% filtered load) **Both technially K+ sparing** Both reduce ENaC activity Both can produce potentially life threatening hyperkalaemia (esp. if used with ACEI or K+ supplements)
46
What are the common uses for Aldosterone antagonists?
**Conn's syndrome:** Spironolactone best drug for Conn's syndrome (Primary hyperaldosteronism) Reduces aldosterone released from adrenal glands (Could be excess in Conn's due to tumour or hyperplasia) **Ascites and oedema in cirrhosis** **Used w/loop diuetics in Heart failure**
47
What classes of diuretic are not currently used as diuretics?
Carbonic anhydrase inhibitors Osmotic diuretics
48
What are the uses of carbonic anhydrase inhibitors and what is one side effect?
**Glaucoma:** Can reduce aqueous humour formation in eye up to 50% **Side effect:** Can cause metabolic acidosis due to HCO3- loss in urine
49
What is an alternative use of Osmotic diuretics?
IV mannitol used to treat cerebral oedema
50
Outline how Nephrotic syndrome causes Oedema and ECF expansion and hence why it is suitable to treat with diuretics
Protein loss in urine Therefore low plasma albumin, low oncotic pressure and oedema occurs Reduced circulating volume activates RAAS and Na+ and water are retained leading to further ECF expansion and oedema Diuretics used to treat (Loop diuretics) and reduce ECF volume
51
Outline why liver cirrhosis is treated with diuretics
Lowered albumin production of liver leads to oedema and reduced circulating volume This in turn activates RAAS, causing ECF expansion and further oedema Also, portal hypertension (Increases GI venous pressure) coupled with low oncotic pressure leads to ascities Fluid loss due to ascites reduces circulatory volume, further activating RAAS and hence ECF expansion and oedema worsens further
52
Outline how loop and thizide diuretics can cause K+ loss and hypokalaemia
By blocking Na+ and water reabsorption in the LoH or Early DCT they increase Na+ and water delivery to the Late DCT/CD **3 Effects of this:** This increases flow rate, washing K+ away from principal cells, increasing the K+ gradient across them Increased absorption of Na+ creates a more favourable electrical gradient for K+ secretion Reduction of ECF due to diuretics activate RAAS and increase aldosteron release, leading to further increased Na+ absorption and K+ secretion **All lead to increased K+ loss leading to hypokalaemia**
53
How do K+ sparing and aldosterone antagonist diuretics cause hyperkalaemia?
**K+ sparing:** Block ENaC **Aldosteron antagonists:** Block action of aldosterone Reduce activity of Na+/K+ ATPase, ENaC and K+ channels on principle cells **Effects:** Both these mechanisms lead to reduced Na+ absorption and K+ secretion Hyperkalaemia results
54
How can we minismise the effects of diuretics on K+ levels?
Monitor electrolytes during diuretic therapy Give K+ supplements with thiazide and loop diuretics Use a combination of K+ sparing or aldosterone and thiazide or loop diuretics to balance effects
55
Whay is spironolactone the preffered drug for treating the oedema and ECF expansion of ascites?
Loop diuretics would be more effective but can cause hypokalaemia Hypokalaemia can precipitate hepatic encephalopathy in a patient with advanced cirrhosis
56
What is hepatic encephalopathy? Hint: Mechanisms and symptoms
**General:** Reversible syndrome of impaired brain function due to advanced liver failure **Mechanism:** Liver not detoxifying ammonia causing elevated serum ammonia levels **Symptoms:** Confusion and coma Constructional apraxia (Cannot build, assemble or draw things), flapping tremors
57
What factors might increase possibility of hyperkalaemia when treting with aldosterone antagonists (spironolactone)
K+ supplements ACEI or Angiotensin receptor blockers Impaired renal function
58
What are some of the adverse effects of diuretics not involving K+?
Hypovolaemia Hyponatraemia Increased uric acid in blood (precipitate gout attack) Metabolic effects (Loop and thiazides): * - Glucose intolerance* * - LDL levels rise* Erectile dysfunction (thiazides)
59
What are some other drugs with diuretic action?
**Alcohol:** Inhibit ADH release **Lithium:** Inhibits ADH action **Coffee (Caffeine):** Increased GFR and decreased Na+ absorption
60
What are some diseases that cause diuresis/polyuria? Mechanisms of each?
**Diabetes mellitus:** Glucose in filtrate, osmotic diuresis **Diabetes insipidus:** Cranial - Decreased ADH release Nephrogenic - Poor ADH response in CD **Psychogenic** Increased water intake

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