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ESA 3 > Urinary 7 > Flashcards

Urinary 7 Flashcards

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
Q

Describe asymptomatic bacteriuria

A

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
Q

What are the general prinicples of UTI treatment?

A

Increase fluid intake

Address underlying disorders

3 day antibiotic course of uncomplicated

5 days for complicated (paeds, pregnant, male, underlying disorder)

27
Q

Outline the treatment of simple cystitis

A

Uncomplicated infection

3 day course of trimethoprim or nitrofurantoin

28
Q

Outline treatment of complicated UTI

A

Trimethoprim, nitrofurantoin or cephalexin for 5 days

Cultures during follow up

29
Q

Outline the treatment of pyelonephritis/septicaemia

A

14 day antibiotic course

Use systemic agent (Co-amoxiclav, Ciprofloxacin, Gentamicin)

IV antibiotics if acutely unwell

30
Q

Outline UTI prophylaxis

When is it used and what is it?

A

When:

3 or more infections in one year

No treatable underlying condition

What:

Trimethoprim or nitrofurantoin

Single nightly dose

All breakthrough infections documented

31
Q

What is a diuretic? What are it’s effects?

A

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
Q

When are diuretics used?

A

In conditions where Na+ and water retention cause ECF expansion (E.g. Heart failure)

33
Q

Outline the general mechanism for Na+ and water reabsorption from the nephron

A

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
Q

Each tubule segments have differnt apical channels/transporters, list which are found in each segment

A

PCT:

Na+/H+ antiporter

Na+ - AA/Glucose symporters

LoH:

Na+/K+/2Cl symporter

Early DCT:

Na/Cl symporter

Late DCT and CD:

ENaC

35
Q

Outline the mechanism of Na+ reabsorption and related processes by principal cells

How can this process be modulated?

A

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
Q

Outline the classes of diuretics that work by direct action on luminal cells

A

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
Q

How do diuretics that work via direct actions on cells exert their effects?

A

Secreted into the lumen in the PCT

Act on cells from within lumen

38
Q

Outline how diuretics that antagonise the action of aldosterone function

A

Aldosterone antagonists reduce expression od Na/K-ATPase, ENaC and K+ channels on principal cells

This reduces Na+ absorption and K+ secretion

39
Q

How do osmotic diuretics work?

A

Freely filtered at glomerulus

Not reabsorbed, remaining in lumen

Increased osmolarity of filtrate leads to reduced water and Na+ reabsorption throughout tubule

40
Q

How do enzyme inhibitor diuretics typically work?

A

Acts on PCT

Inhibition of carbonic anhydrase:

- Enzyme that catalyses H2O + CO2 HCO3- + H+

Interferes with Na+ and HCO3- reabsorption

41
Q

Give the 6 groups that diuretics are classified into and give examples of each

A

Loop diuretics:
Furosemide

Thiazide diuretics:
Bendroflumethiazide

K+ sparing diuretics:
Amiloride

Aldosterone antagonists:
Spironolactone

Carbonic anhydrase inhibitors:
Acetazolamide

Osmotic diuretics:
Mannitol

42
Q

Describe why loop diuretics are so potent

A

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
Q

What are some uses of Loop diuretics?

A

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
Q

Dscribe the potency of thiazide diuretics

Give uses

Give common side effects

A

Potency:

Only inhibits 5% of Na+ reabsorption

Uses:

Hypertension (also cause vasodilation)

Side effects:

Higher incidence of hypokalaemia

Increases Ca2+ absorption

45
Q

What are the similarities between K+ sparing diuretics and Aldosterone antagonists?

A

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
Q

What are the common uses for Aldosterone antagonists?

A

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
Q

What classes of diuretic are not currently used as diuretics?

A

Carbonic anhydrase inhibitors

Osmotic diuretics

48
Q

What are the uses of carbonic anhydrase inhibitors and what is one side effect?

A

Glaucoma:

Can reduce aqueous humour formation in eye up to 50%

Side effect:

Can cause metabolic acidosis due to HCO3- loss in urine

49
Q

What is an alternative use of Osmotic diuretics?

A

IV mannitol used to treat cerebral oedema

50
Q

Outline how Nephrotic syndrome causes Oedema and ECF expansion and hence why it is suitable to treat with diuretics

A

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
Q

Outline why liver cirrhosis is treated with diuretics

A

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
Q

Outline how loop and thizide diuretics can cause K+ loss and hypokalaemia

A

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
Q

How do K+ sparing and aldosterone antagonist diuretics cause hyperkalaemia?

A

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
Q

How can we minismise the effects of diuretics on K+ levels?

A

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
Q

Whay is spironolactone the preffered drug for treating the oedema and ECF expansion of ascites?

A

Loop diuretics would be more effective but can cause hypokalaemia

Hypokalaemia can precipitate hepatic encephalopathy in a patient with advanced cirrhosis

56
Q

What is hepatic encephalopathy?

Hint: Mechanisms and symptoms

A

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
Q

What factors might increase possibility of hyperkalaemia when treting with aldosterone antagonists (spironolactone)

A

K+ supplements

ACEI or Angiotensin receptor blockers

Impaired renal function

58
Q

What are some of the adverse effects of diuretics not involving K+?

A

Hypovolaemia

Hyponatraemia

Increased uric acid in blood (precipitate gout attack)

Metabolic effects (Loop and thiazides):

    • Glucose intolerance*
    • LDL levels rise*

Erectile dysfunction (thiazides)

59
Q

What are some other drugs with diuretic action?

A

Alcohol:

Inhibit ADH release

Lithium:

Inhibits ADH action

Coffee (Caffeine):

Increased GFR and decreased Na+ absorption

60
Q

What are some diseases that cause diuresis/polyuria?

Mechanisms of each?

A

Diabetes mellitus:

Glucose in filtrate, osmotic diuresis

Diabetes insipidus:

Cranial - Decreased ADH release

Nephrogenic - Poor ADH response in CD

Psychogenic

Increased water intake

ESA 3 (54 decks)

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