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Semester 3 > Renal& UTIs > Flashcards

Renal& UTIs Flashcards

1
Q

What anatomical feature in females means UTIs are more common?

A

Shorter urethra

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2
Q

What are the host factors contributing to UTIs?

A

Shorter urethra
Obstruction - enlarged prostate, pregnancy, stones, tumour
Neurological problems - incomplete emptying, residual urine
Ureteric reflux - ascending infection from bladder esp in children

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3
Q

WHere are common sites of urinary tract obstruction?

A 
PUJ: calculi
Ureter: Calculi, Ca, retroperitoneal fibrosis
Bladder: Neuropathic bladder
VUJ: calculi
Bladder neck: hypertrophy
Prostate: BPH/Ca
Urethra: stricture
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4
Q

What are the bacterial factors of UTIs?

A

Fimbrae allow attachment to host epithelium
K antigen permits production of polysaccharide capsule
Urease breaks down urea creatinga favourable environment for bacterial growth
Haemolysins damage host membranes and cause renal damage

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5
Q

What are the clinical syndromes of a UTI?

A 
Frequency and dysuria (lower UTI)
Acute pyelonephritis (upper UTI)
Chronic nephritis 
Asymptomatic (pregnancy many problems for mother and baby) 
Septicaemia +/- shock
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6
Q

What are the signs and symptoms of a lower UTI?

A

Low grade fever
Dysuria
Frequency
Urgency

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7
Q

What are the signs and symptoms of an upper UTI (pyelonephritis)?

A

Fever
Loin pain
May have dysuria, frequency

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8
Q

When are investigations of UTI needed?

A

Healthy women - ‘uncomplicated UTI’ no need to culture urine - nitrite/leucocyte esterase dipstick testing
Culture urine in ‘complicated UTI’ ie pregnancy, treatment failure, suspected pyelonephritis, complications, male, paediatric

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9
Q

How might a specimen be collected to investigate a UTI further?

A 
MSU - cleansing not required in women
Clean catch in children - no antiseptic
Collection bag (20% false positives)
Catheter sample
Supra-pubic aspiration
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10
Q

How is a specimen for UTI investigation transported?

A

4 degrees C +/- boric acid - disolves in the urine, stops the microorganisms multiplying -> accurate results

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11
Q

What can be tested in a urine sample?

A 
-Turbidity (visual inspection)
DIpstick testing can detect:
-Leucocyte esterase
-Nitrite
-Haematuria
-Proteinuria
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12
Q

What cells will be present in a urine sample of a patient with a UTI under the microscope?

A

Acute - WBC and RBC

Contaminated urine - squame (epithelial cells) NOT indication of UTI

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13
Q

Why is a nitrite test specific but not sensitive for UTI investigation?

A

Specific - if nitrites present in sample, definite positive test for UTI
Sensitive - Not all bacteria produce nitrites therefore not all UTIs will produce nitrite positive test

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14
Q

What might make a urine culture tray turn pink?

A

Lactose fermentors change pH

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15
Q

How many colonies distinguishes bacteriuria and when is this useful?

A

> 10^5 cfu/ml

Asympomatic females compared with femals with pyelonephritis

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16
Q

What is the role of a culture of urine?

A 
Investigation of children, males and comlicate infections
Increased sensitivity
Epidemiology of isolates
Susceptible data
Control of specimen quality
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17
Q

What needs to be taken into account in interpretation of a culture report for a UTI?

A 
Clinical details - symptoms/previous antibiotics
Quality of specimen
Delays in culture
Microscopy (if available)
Organism(s) isolated
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18
Q

What other problems may be the cause of urethral syndrome?

A 
Low bacteriuria
Fastidious organism
Vaginal infection/inflammation
STI - urethritis
Mechanical, physical and chemical causes
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19
Q

When would imaging of the urinary tract be used?

A

All children
Males - posterior urethral valves
Females - vesico- ureteric reflux

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20
Q

What might sterile pyuria be indicative of?

A 
Antibiotics 
Urethritis 
Vaginal infection/inflammation
Chemical inflammation
TB
Appendicitis
Fastidious organism?
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21
Q

What is the treatment of a UTI?

A

Increases fluid intake
Adress underlying disorders
3 day antibiotics if uncomlicated, 5 if complicated
CSU only if symptomatic - likely false positive as it is another medium for bacteria to colonise

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22
Q

What is the treatment of simple cystitis?

A

Uncomplicated infections can be treated with trimethoprim or nitrofurantoin.
3 day course as effective as 5/7 os use minimal to reduce resistance

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23
Q

What antibiotics are used for complicated UTIs?

A

Trimethoprim, nitrofurantoin or cephalexin

Amoxicillin not appropriate as 50% resistant

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24
Q

How is pyelonephritis/septicaemia treated?

A

14 day course
Agent with systemic activity
Possibly IV initially unless good PO absorption and patient well enough
Co-amoxiclav, ciprofloxacin, gentamicin (IV only - nephrotoxic)

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25
Q

Why is ciprofloxacin rarely used anymore?

A

Commonly results in C. diff

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26
Q

When would prophylaxis be given to a patient for UTI?

A

More than 3 episodes in 1 year
No treatable underlying cause
Trimethoprim or nitrofurantoin - single nightly dose

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27
Q

What are the problems of prophylaxis for recurrent UTIs?

A

Resistance builds

Expensive

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28
Q

What is diuresis?

A

Increased formation of urine by the kidney

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29
Q

What is a diuretic?

A

A substance that promotes a diuresis -> reduction in ECF volume. Increase fraction excretion of sodium by blocking reabsorption

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30
Q

When are diuretics used?

A

Conditions with ECF expansion and oedema
Acute pulmonary oedema
Hypertension
(Na and water reabsorption too high)

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31
Q

As well as blocking ENaC in the luminal membrane of the DCT and CD, what else do diuretics do here?

A

Reduce K+ secretion - disruption of electrochemical gradient

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32
Q

What diuretics are used?

A
  1. Direct action on cells to block Na+ transporters in the luminal membrane
  2. By antagonising action of aldosterone
  3. Thiazide diuretics
  4. K+ sparing
  5. Modification of filtrate content - osmotic diuretics
  6. Inhibition of carbonic anhydrase inhibitors (no longer used as diuretic)
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33
Q

What diuretics work on the DCT?

A

Thiazide diuretics
Metalozone
Indapimide

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34
Q

What type of diuretics are used on the late DCT and CD?

A

K+ sparing diuretics

Aldosterone antagonists

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35
Q

How do antagonising aldosterone diuretics work?

A

Inhibits aldosterone action on principle cells of late DCT and CD reducing Na reabsorption. Competitive inhibition

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36
Q

How do osmotic diuretics work?

A

Increase osmolarity of filtrate by reducing reabsorption out of tubule

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37
Q

How could carbonic anhydrase inhibitors be used as a diuretic?

A

Acts on PCT inhibiting carbonic anhydrase interferes with Na and HCO3- reabsorption -> can cause metabolic acidosis
Useful in treatment of glaucoma -> reduces formation of aqueous humor in eye by about 50%

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38
Q

Where do loop and thiazide diuretics enter the tubule?

A

PCT via organic anion pathway -> travel downstream to loop/DCT

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39
Q

Why are loop diuretics so potent?

A

25-30% of Na reabsorbed in loop

Segements beyond have limited capacity to reabsorb the resulting Na and H2O

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40
Q

When are loop diuretics used?

A 
Heart failure
Treat flui dretention and oedema in:
- nephrotic syndrome
- renal failure
- cirrhosis of liver 
Impairs calcium absorption in the loop of henle  - useful to treat hypercalcaemia
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41
Q

How do thiazide diuretics work?

A

Block Na-Cl transporter in DCT. Less potent than loop, less Na reabsorption in DCT

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42
Q

When are thiazide diuretics used?

A

Hypertension (vasodilation

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43
Q

What problems are associated with thiazide diuretics?

A

Hypokalaemia (also associated with K sparing diuretics)

esp if used with ACE inhibitors, K supplements or in patient with renal impairment

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44
Q

What is the best drug treatment of hypertension due to primary hyperaldosteronism (Conn’s syndrome)?

A

Aldosterone antagonists

Also used for ascites and oedema in cirrhosis and in addition to loop diuretics in heart failure

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45
Q

How does mannitol work as an osmotic diuretic?

A

Small inert molecule
Increase plasma osmolarity thus drawing out fluid from tissues and cells
Freely filtered at the glom. but not reabsorbed -> increases osmolarity of filtrate
Acts by altering the driving force for renal absorption (osmolarity)
Loss of water, Na and K

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46
Q

When is oedema common?

A

Congestive heart failure - increase in venous pressure. Drop in CO causes activation of RAAS
Nephrotic syndrome
Cirrhosis of liver
Kidney failure

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47
Q

How does nephrotic syndrome cause oedema?

A 
Protein los in urine
Low plasma albumin
Low oncotic pressure -> oedema
Reduced circulatory vol
RAS activated
Na and H2O retention 
Expansion of ECF and oedema
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48
Q

How does cirrhosis of the liver cause oedema?

A

Less albumin production in liver so low in plasma
Low oncotic pressure -> oedema
Reduced circulatory volume
RAS activated
Na and water retention -> expansion of ECF and worsening oedema

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49
Q

How does liver cirrhosis cause ascites?

A

Portal hypertension -> increased venous pressure in splanchnic circulation (high venous pressure + low oncotic pressure ->ascites)
Reduced circulatory volume activates RAS and Na and water retained causing expansion of ECF and worsening oedema

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50
Q

What alternative uses do diuretics have?

A

Hypercalcaemia treatment - loop diuretics
Mannitol used in cerebral oedema
Treat glaucoma with carbonic anhydrase inhibitors

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51
Q

Define micturation.

A

To want to pass urine

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52
Q

Define detrusor

A

To push down

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53
Q

What controls micturation?

A

The spinal cord

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54
Q

What are the functional divisions of the bladder?

A

Body - Temporary store of urine
Trigone - ureteric orifices and internal urethral orifice are at angles of a triangle
Neck - Connects bladder to the urethra

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55
Q

What are the 3 major muscles in the bladder?

A

Detrusor urinae
Internal urethral sphincter
External urethral sphincter (formed by pelvic floors)

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56
Q

Describe arrangement of the detrusor muscle.

A

Formed from a plexiform meshwork of smooth muscle fibres
Appear in random distribution in orientation in cross section but actually in 3 layers - inner longitudinal, middle circular, outer longitudinal
Strength

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57
Q

What type of neural supply supplies the detrusor urinae muscle?

A

Bilateral (left and right sides of the spinal cord)
Various anatomical components of the bladder are supplied by different divisions of the nervous system -> disorders can be varied and complex
Autonomic symp and para
Not voluntary control

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58
Q

What nervous supply is the external urethral sphincter?

A

Somatic. Voluntary control from cerebral cortex via the spinal cord

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59
Q

Why are neuronal disorders of the urinary bladder very complex?

A

Spinal lesions controlling the bladder disturbs the ordered co-operation between the somatic and autonomic divisions of the nervous system
Can be life threatening

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60
Q

What are the characteristics of the detrusor muscle?

A 
Classified as smooth muscle 
A mass of contracting muscle
Has no peristaltic activity
Lined with transitional epithelium
Epithelium of bladder is non-secretory
Same form and size in both sex
Found in the true pelvis
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61
Q

What are the general functions of the urinary bladder?

A

Temporary storage of urine

Expulsion of urine

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62
Q

What is the continence phase?

A

Storage of urine

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63
Q

What results from neuronal apparatus damage?

A

Failure to store urine resulting in reduced bladder capacity, hence very frequent passing of urine - incontinence

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64
Q

What is the micturation phase?

A

Voiding function of the urinary bladder
Damage to neurones that promote micturation will lead to failure to pass urine voluntarily resulting in urine retention. Urine is then only passed by an overflowing bladder

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65
Q

Describe the coordination of neural control required to pass urine.

A

Bladder and external urethral sphincter must coordinate. Bladder relaxes, sphincter contracts. Bladder contracts, sphincter relaxes
Disturbances in this synchrony leads to detrusor-Sphincter dussenergia

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66
Q

What are continence circuits?

A

Neural apparatus prescribing for urinary storage

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67
Q

What is the capacity of the bladder?

A

approx 550ml (300-700 sometimes up to 1L)

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68
Q

What is monitored in the bladder?

A

Urine ionic composition, temp, volume by sensory neurones in submucosa

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69
Q

How is continence controlled?

A

Sympathetic
Cerebral cortex -> Pontine continence or storage centre (L-region) -> Sympathetic nuclei in cord -> Detrusor muscle and sphincter motorneurones in sacral cord

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70
Q

What receptors bring about relaxation of the detrusor muscle?

A

Beta 3 in the funds and body of bladder

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71
Q

What receptors increase the urethral sphincter pressure?

A

Alpha adreno in neck

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72
Q

What branch of the nervous system activates closure of the external urethral sphincter?

A

Somatic

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73
Q

What are the root values of the sympathetic nervous system?

A

Thoraco-lumbar - T10/12 - L2
Derived from lumbar splanchnics
T10-12 terminate in the inferior mesenteric ganglion
L1 and 2 terminate on neurones of the hypogastric plexus or presacral nerves

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74
Q

Where does the somatec nervous system originate from?

A

Onlufs nucleus of the ventral horn of the cord

S2-4

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75
Q

What are the folds in the bladder known as?

A

Rugae

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76
Q

What are the mechanical events during continence and storage?

A

Internal urethral sphincter tightens/closes - somatic
Rugae flatten - capacity increases - sympathetic
Intravesical pressure hardly changes - sympathetic

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77
Q

What results from bilateral lesions in the PSC?

A 
Inability to store urine
Reudction in capacity
Excessive detrusor muscle activity
Relaxation of urethra
Premature voiding
Leaky bladder
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78
Q

Where do afferent nerves originate in the urinary tract?

A 
Bladder wall
Thought to be stretch receptors but unknown
Travel principally with para
Some limited routing with sympathetic
Pain sensation well localised
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79
Q

What are the signals the bladder needs to be void?

A

Paina and sensation from irritation of bladder

Temperature sensation

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80
Q

What mediates voiding of the bladder?

A

Independent neural apparatus

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81
Q

What is the flow rate of urine?

A

20-25 ml/s in men 24s

25-30 ml/s in women 22s

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82
Q

What is the threshold for feelings suggestive of a full bladder?

A

approx 400ml

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83
Q

What is the neural apparatus prescribing voiding of the bladder known as?

A

Voiding circuits. Controlled by micturition centres of the spinal cord. Mediated exclusively by parasympathetic neurones of the sacral division of the spinal cord

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84
Q

What do voiding circuits do?

A

Stong contraction of detrusor mucle
Increase in intravesical pressure
Relaxation of the internal urethral spincter
Voluntary relaxation of the external urethral sphincter
Expulsion of urine

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85
Q

Where do voiding circuits arise from?

A

Cerebral cortex -> The pons -> sacral levels of parasympathetc outflow -> detrusor muscle contracts -> external sphincter relaxes

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86
Q

What roots are involved in the mechanism of urinary voiding?

A

Cerebral cortex - somatic S2-4 (ventral horn) relaxes/opens ex urethral spincter
Parasympathetic division of ANS - S2-4 (lateral horns) increase detrusor activity

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87
Q

Why do sensation and voiding of the bladder not need to be under conscious control?

A

No sensory representation of the bladder in the sensory cotex
No motor representation of the bladder in the motor cortex
Nerve supply to the bladder is all by the ANS

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88
Q

What nerve supplies the external urethral sphincter?

A

Perineal branch of the pudenal nerve S2-4
Constricts urethra for maintenance of continence
Relaxation promotes voiding

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89
Q

What wil lower motor neurone lesion of S2,3,4 cause?

A

Reduced periana lsensation. Lax anal tone. Low detrusor pressure
Large residual urine +/- overflow incontinence

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90
Q

What do upper motor neurone lesions of S2,3,4 cause?

A

Dilated ureters
Thickened detrusor
High pressure detrusor contractions
Poor coordination with sphincters - DETRUSOR SPHINCTER DYSSYNERGIA

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91
Q

WHat are the symptoms of LUTS?

A

Frequency, urgency, nocturia, incontinence
Slow stream, splitting or straying, intermittency
Hesitancy, Straining, Terminal dribble
Post-micturition dribble, feeling of incomplete emptying

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92
Q

How is urinary incontinence defined?

A

The complaint of any involuntary leakage of urine

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93
Q

Name some types of UI.

A

Stress UI - on effort or exertion or on coughing or sneezing
Urge UI accompanied by or immediately proceeded by urgency
Mixed UI - both
Overflow incontinence

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94
Q

Is overactive bladder syndrome or UUI more prevalent?

A

OAB - wet and dry.

95
Q

What are the symptoms of OAB?

A

Urgency
Frequency
Nocturia

96
Q

What are the incidence rates of UIs?

A

28% MUI
47% SUI
21% UUI
4% other

97
Q

What are the risk factors for UUIs?

A 
pregnancy and childbirth
pelvic surgery/DXT
Pelvic prolapse
Race
Genetics
Anatomical/neurological abnormalitie
Co-morbidities
Obesity
Age
Increased intra-abdo pressure
cognitive impairment
Menopause
Drugs
UTI
98
Q

What examinations are done to diagnose the cause of UI?

A

Height
Weight
Abdominal exam to exclude palpable bladder
Digital rectal examination - prostate, limited neurological examination
Females - external genitalia (stress test) and vaginal exam

99
Q

What are the mandatory investigations for UIs?

A

Urine dipstick - UTI, haematuria, proteinuria, glucosuria

100
Q

What other investigations can be done for UIs?

A

Basic non-invasive urodynamics - frequency-volume chart, bladder diary, post-micturation residual volume in patients with voiding dysfunction
Optional - invasive urodynamics, pad test, cystoscopy

101
Q

What does management of UTI depend on?

A

Which symptoms
Degree of bother/nuisance
Effects of treatment on other symptoms
Previous or current treatments

102
Q

What conservative management of UUIs is used?

A 
Modify fluid intake
Weight loss
Stop smoking
Decrease caffeine intake
Avoid constipation
Timed voiding - fixed schedule
103
Q

What treatment can be given for patients unsuitable for surgery?

A

Indwelling catheter - urethral or suprapubic
Sheath device - analogous to an adhesive condom attached to catheter tubing and bag
Incontinence pads

104
Q

What is the initial management of an SUI?

A

Pelvic floor muscle training - 8 contractions x3/day at least 3 month duration

105
Q

What are the pharmacological managements of SUIs?

A

Duloxetine - combined noradrenaline and serotonin uptake inhibitor increases activity in the striated sphincter during filling phase
Not recommended by NICE as first-line or routine second line treatment but may be offered as an alternative to surgery

106
Q

What surgical procedures can be used to treat SUIs in females?

A

Permanent intention:
Low-tension vaginal tapes (commonest)
Open retropubic suspension procedures - correct anatomical position of proximal urethra and improve urethral support
Classical sling prcedures

Temporary intention:
Intramural bulking agents - improve ability of urethra to resist abdominal pressure by improving urethral coaptation.

107
Q

Describe the surgery used to treat SUIs in males.

A

Male sling procedure - experimental, bone bone-anchored tape, minimally invasive. Long term results unknown
Artificial urinary sphincter - gold standard

108
Q

Describe low-tension vaginal tapes.

A

Supports mid urethra
Polypropylene mesh
Minimally invasise - Tension-free vaginal tape or Transurator tape
Success rate >90%

109
Q

How does classical fascial sling procedures correct SUIs?

A

Supports urethra and augments bladder outflow resistance.
Autoglass - fascia lata/rectus fascia
Allograft fascia lata

110
Q

What agents can be used for intramural bulking?

A

Injection under GA/LA of autologous fat, silicone, collagen or hyaluron-dextran polymers

111
Q

How does a male artificial urinary sphincter work?

A

Cuff stimulates action of normal sphincter to circumferentially close the urethra
Mechanical (hydraulic) device
Infection, erosion and device failure

112
Q

What usually causes SUIs in men?

A

Usually iatrogenic:

  • Radical prostatectomy
  • Colorectal surgery
  • Radical pelvic radiotherapy
113
Q

What is the initial management of UUI?

A

Bladder training - schedule of voiding.
Void every hour during the day, must not void in between - wait or leak
Intervals increased by 15-30 mins/week until intervals of 2-3 hrs.
At least 6 week duration

114
Q

What is the pharmacological management of UUIs?

A 
Anticholinergics - act on muscarinic receptors (M2, M3) - Oxybutynim
Botulinum toxin (neurotoxin). Inhibits release of Ach at pre-synaptic neuromuscular junction causing targeted flaccid paralysis. Mainly type A for 3-6 months
115
Q

What are the potential side effects of anticholinergic drugs for UUI management?

A 
Side effects due to affects on M receptors at other sites
M1 - CNS, salivary glands
M2 - Heart smooth muscle
M3 - smooth muscle, salivary glands
M4 - CNS
M5 - CNS, eyes
116
Q

What surgical treatment can be given for UUI?

A

Sacral nerve neuromodulation
Autoaugmentation
Augmentation cystoplasty
Urinary diversion

117
Q

Describe sacral nerve neuromodulation.

A

Stimulation of S3/4 to modulate the reflexes responsible for involuntary bladder contraction. Precise mechanism unknown
Initial percutaneous nerve evaluation (PNE)
Implanted electrode and battery powered generator - 7yr life
Problems: infection requiring removal, device failure

118
Q

Describe autoaugmentation.

A

Aim to increase functional capacity and decrease intravesical pressure created by involuntary detrusor contractions. Not widely used. Mainly neurogenic cases of OAB with UUI

Detrusomyectomy - large disc of detrusor removed from dome
Detrusomyectomy - incision through detrusor muscle with edge everted

119
Q

Describe augmentation cystoplasty.

A

Aim to increase functional capacity. Bladder bivalved and detubularised bowel segment is anastamosed

120
Q

What are the problems with with augmentation cystolplasty?

A 
Need to self catheterise
UTIs
Mucous
Stones
Metabolic abnormalities
121
Q

Describe urinary diversion (ileal conduit).

A

Segment of ileum excised on its pedicle
Ureters transected and anastamosed to proximal end of ileal segment
Distal end of ileal segment brought out as abdominal wall stoma
+/- cystectomy

122
Q

Where is a diabetic most likely to develop renal failure?

A

Perfusion - pre-renal renal failure

123
Q

What may cause prerenal failure?

A

Reduced blood flow to the kidney:
Low volume/pressure
Heart failure
Renal artery stenosis

124
Q

What are the risk factors of AKI?

A

Diabetes
Infection
Drugs
Chronic kidney disease

125
Q

What past medical history will increase the risk of AKI?

A

Diabetes
Hypertension
Hypercholesterolemia
Chronic disease

126
Q

What drugs increase the risk of AKI?

A 
New meds
ACE-I ARBs
NSAIDs
Lithium
Immunosuppressive/ chemotherapy agents
127
Q

What examinations would be undertaken to diagnose AKI?

A 
BP
Skin
CVS
Resp
GI
UGS
CNS 
MS
128
Q

What is suggestive on a dipstick test of renal failure?

A

Blood

Protein

129
Q

What would be seen in a urine microscopy of a patient with AKI?

A

Monomorphic red cells - ureters/collecting duct/pelvis
Red cell cast - glomerulus
Muddy brown granular cast - tubules

130
Q

WHat might cause post renal AKI?

A

Protatic problems
Tumours
Stones

131
Q

What might cause intrinsic renal AKI?

A

Established acute tubular necrosis
Vascular - renal vein thrombosis, artery occlusion, small vessel probs
Interstitial nephritis
Bilateral severe pyelonephritis

132
Q

List some complications of AKI

A 
Acidosis
Pericarditis
Pericardial effusion
Arrythmias
Pulmonary oedema
Gastritis
Malnutrition
GI bleed
Nausea
Irritable
Seizures
Conscious level decreased
Asterixis
Anaemia
bleeding
133
Q

What is the management of AKI?

A 
Treat underlying cause
Fluid replacement
Correct electrolyte disturbances
Correct metabolic acidosis
Nutrition
Volume overload
134
Q

What are the indications that a patient may need dialysis?

A 
Symptomatic uraemia
Hyperkalaemia refactory treatment
Metabolic acidosis refactory treatment
Volume overload refactory treatment
Pericardial involvement
135
Q

What are the outcomes of AKI?

A

5% irreversible
5% initially recover then progress
If recovered 50% residual damage (often subclinical)
Mortality >50% if RRT required

136
Q

What in the urine is sensitive for glomerular nephritis?

A

Blood and protein
NOT specific
Hypertension also common

137
Q

What are red cell casts?

A

A mold of the inside of the nephrons tubule seen in the urine. Shows glomerular bleeding/nephritis

138
Q

Why might microscopic haematuria be present?

A 
Polycystic kidneys
Renal stones
Renal tumours
Arteriovrnous malformations
Glomerular disease
139
Q

What is the first investigation for a patient >45 who has been ruled out for UTI?

A

Cystoscopy - check for renal cell carcinoma

Ultra sound also done

140
Q

What is overt proteinuria?

A

Positive dipstick test. >300mg/day

Microalbuminuria not visible on dipstick

141
Q

What might cause episodic macroscopic haematuria?

A

Brown or smoky in colour if associated with glomerular disease
IgA nephropathy
Renal malignancy must be ruled out
Clots v unusual

142
Q

What other causes are there of red/brown urine?

A

Haemoglobinuria
Myoglobinuria
Consumption of food

143
Q

WHat is the classic triad of findings of nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema
+ hyperlipidaemia

144
Q

What is required to diagnose nephrotic syndrome?

A

Renal biopsy (pathognomonic of glomerular disease)

145
Q

Why is there such a risk in renal biopsy?

A

Kidney takes 20% of cardiac output, renal disease associated with hypertension

146
Q

What is the clinical presentation of nephrotic syndrome?

A 
Oedema
Muercke's bands
Xanthelasma
Fat bodies in urine
(hyperlipidaemias)
DVT - loss of components of coagulation cascade -> procoagulant
147
Q

What are the 3 most common causes of nephrotic syndrome?

A

Minimal change disease (kids)
FSGS - focal segmental glomerulosclerosis
Membranous

148
Q

What is the classic nephritic syndrome?

A

That which accompanies post-streptococcal glomerulonephritis in children
Can be as a result of other glomerulonephritides
Often self-limiting

More commonly now due to vasculitis or lupus

149
Q

What does nephritic syndrome manifest as?

A 
Rapid onset
Oliguria
Hypertension
Generalised oedema
Haematuria with smoky brown urine
Normal serum albumin
Variable renal impairment
Urine contains blood protein and red cell casts
150
Q

What might glomerulonephritides cause?

A

Nephritic or nephrotic syndrome

151
Q

What is the difference between a nephrotic and nephritic patient?

A

Nephrotic - Massive proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia

Nephritic - Haematuria, oliguria, azotemia, hypertenison

152
Q

What does a rapidly progressive glomerulonephritis describe?

A

A clinical situation in which glomerular injury is so severe that renal function deteriorates over days
Patient may present as a uraemic emergency with evidence of extrarenal disease
Associated with crescentic glomerulonephritis
Renal biopsy required for diagnosis
Aka crescentic glomerular nephritis

153
Q

What might a patient with chronic kidney disease (slowly progressive renal impairment) present with?

A

Renal impairment
Hypertension and dipstick abnormalities
Uraemic syndrome
On examination, will not feel anything in abdomen - kidneys usually cannot be felt easily but w/ chronic kidney disease, they are smaller so cannot be felt

154
Q

What are the symptoms of chronic kidney disease?

A 
Tiredness and lethargy
Breathlessness
Nausea and cvomiting
Aches and pains
Sleep reversal
Nocturia
Restless legs
Itching
Chest pains
Seizures and coma
155
Q

What is the treatment of chronic kidney diseae?

A

ACE inhibiter, ARB - reduce protein in urine and help manage hugh blood pressure

156
Q

Why is protein in the urine harmful?

A

Causes inflammation in the kidney -> scar tissue -> reduce function…

157
Q

What pathologies might occur in the filter?

A

Block -Renal failure - decreased eGFR

Leak -Proteinuria (nephrotic syndrome)/haematuria (nephritic syndrome)

158
Q

Where is the likely site of injury if proteinuria occurs?

A 
Podocyte/subepithelial damage
Primary causes:
- minimal change glomerulonephritis
- focal segmental glomerulosclerosis
membranous glomerulonephritis
Secondary causes:
- diabetes mellitus
- (Amyloidosis)
159
Q

When is minimal change glomerulonephritis likely to occur?

A

Childhood/adolescence, incidence reduces with increasing age

160
Q

What are the symptoms of minimal change proteinuria?

A

Heavy proteinuria or nephrotic syndrome

161
Q

What is the treatment of minimal change glomerulonephritis?

A

Responds to steroids
May recur
Usually no progression to renal failure

162
Q

What is the pathogenesis of minimal change glomerulonephritis?

A

Unknown circulating factor damaging podocytes

No immune complex deposition

163
Q

How is focal segmental glomerulosclerosis different to minimal change glomerulonephritis?

A 
Nephrotic
Occurs in adults
Less responsive to steroids
Glomerulosclerosis
Circulating factor damaging podocytes -> transplant
Progressive to renal failure
164
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis - immune complex deposits, probably autoimmune, may be secondary (associated with other pathologies e.g. lymphoma)

165
Q

What is the prognosis of membranous glomerulonephritis?

A

Rule of thirds:

  1. 1/3 of patients will have spontaneous remission
  2. 1/3 of patients will have persistent proteinuria but stable renal function
  3. 1/3 of patients will have progressive loss of GFR
166
Q

What problems can diabetes mellitus cause in the kidneys?

A 
Progressive proteinuria
Progressive renal failure
Microvascular
Mesangial sclerosis -> nodules
Basement membrane thickening
167
Q

What causes haematuria?

A

Thin glomerular basement membrane disease/Hereditary Nephropathy (Alport)
IgA nephropathy

168
Q

What causes nephritic syndrome?

A

Good pasture syndrome (Anti-GBM disease)

Vasculitis

169
Q

Describe IgA nephropathy.

A

Commonest GN
Any age
Classically present with visible/invisible haematuria
Relationship with mucosal infection
Variable histological features and course (mesangial damage, immune complex deposition - containing IgA)
+/- proteinuria
Significant proportion progress to renal failure
No effective treatment

170
Q

Name 2 hereditary nephropathies

A

Thin GBM

Alport

171
Q

What is the pathology of thin GBM?

A

Benign familial nephropathy
Isolated haematuria
Thin GBM
Benign course

172
Q

What is the pattern of inheritance and pathology of Alport’s syndrome?

A 
X linked
Abnormal collagen IV
Associated with deafness
Abnormal appearing GBM (split and laminated)
Progresses to renal failure
173
Q

Describe Goodpasture syndrome (anti-GBM)

A

Relatively uncommon though clinically important
Rapidly progressive GN
Acute onset of severe nephritic syndrome
Classically described association with pulmonary haemorrhage (smokers)
Autoantibody to collagen IV in basement membranes (?)
Treatable by immunosupression and plasmaphoresis if caught early

174
Q

Describe vasculitis.

A 
Group of systemic disorders 
No immune complex/antibody deposition
Association with Anti Neutrophil Cytoplasmic Antibody
Nephritic presentation
Treatable if caught early
Urgent biopsy service
175
Q

What are the risk factors of prostate cancer?

A

Increasing age
Family history (x4). BRCA2 gene mutation
Ethinicity - black > white > Asian

176
Q

What is the NHS official policy on prostate cancer risk management?

A

Does not recommend mass population screening

Supports opportunistic screening if patients are counselled

177
Q

What are the issues for PSA screening?

A

Overdiagnosi
Over-treatment
QoL - co-morbidities of established treatments
Cost-effectiveness

178
Q

What are the clinical presentations of prostate cancer?

A

Asymptomatic
Urinary symptoms - benign enlargement of prostate/bladder overactivity +/- CaP
Bone pain
Occasionally haematuria (in advanced CaP)

179
Q

What is the diagnostic pathway for prostate cancer?

A

Digital rectal examination (DRE), serum PSA (prostate specific antigen) -> TRUS (transrectal ultrasound) - guided biopsy
Lower urinary tract symptoms -> Transurethral reaction of prostate (TURP)

180
Q

What are the factors influencing treatment of prostate cancer?

A

Age
DRE - localised (T1/T2) / locally-advanced (T3) / Advanced (T4)
PSA level
Biopsies - gleason grade / extent
MRI scan and bone scan - Nodal and visceral metastases

181
Q

What is the treatment of a localise CaP?

A

Surveillance
Radical prostectomy - open/ laproscopic/ robotic
Radiotherapy - External beam/ low dose rate brachytherapy

HIFU
Primary cryotherapy
High dose rate brachytherapy

182
Q

How is metastatic CaP treated?

A

Hormones - surgical castration/ medical castration - LHRH agonists
palliation - single-dose radiotherapy/ bisphosphonates (zoledronic acid)/ chemotherapy (docetaxel)

183
Q

When are bone metastases common from prostate cancer?

A

If PSA >10 ng/ml
Sclerotic (osteoblastic)
Hot spots on bone scan

184
Q

What is the treatment for locally advanced CaP?

A

Surveillance
Hormones
Hormones and radiotherapy

185
Q

How is haematuria classified?

A

Visible

Non visible - dipstick / microscopic

186
Q

What are the differential diagnoses of haematuria?

A 
Cancer - renal cell carcinoma, upper tract transitional cell carcinoma, bladder cancer, advanced prostate carcinoma
Stones
Infection
Inflammation
Benign prostatic hyperplasia (large)
Nephrological (glomerular)
187
Q

What examinations would be done on a patient with haematuria?

A 
BP
Abdominal mass
Varicocele
Leg swelling
Assess prostate by DRE (size/texture)
188
Q

What investigations would due done on a patient with haematuria?

A

Blood - FBC, U&E
Radiology - ultrasound, IVU
Endoscopy - Flexible cystoscopy
Urine - culture and sensitivity, cytology

189
Q

What is the most common type of bladder cancer?

A

transitional cell carcinoma (90%)

190
Q

What are the risk factors for bladder cancer?

A

Smoking x4
Occupational exposure - rubber or plastic manufacture , handling carbon, crude oil, combustion, smelting (polyaromatic hydrocarbons)
Painters, mechanics, printers, hairdressers
Schistosomiasis

191
Q

What is the initial definitive treatment of bladder tumour?

A

TUR (transurethral resection)
Superficial TURBT
Separate deep TUR of muscle
Single intravesical instillation of mitomycin C

192
Q

How many bladder cancers are superficial/muscle invasive?

A

75% superficial
20% muscle invasive
5% carcinoma in situ (Tis)

193
Q

What further treatment is given to patients with high risk non muscle-invasive TCC?

A

Check cystoscopies

Intravesical immunotherapy

194
Q

What further treatment is given to patients with lower risk non muscle-invasive TCC?

A

Check cystoscopies

+/- intravesical chemotherapy

195
Q

What further treatment is given to patients with muscle-invasive TCC?

A

+/- Neoadjuvant chemo
+ radical cystectomy or radiotherapy to cure.
1 treatment not curative

196
Q

What is a radical cystectomy?

A

Operation to remove the bladder urethra, lymph nodes and seminal vesicle/part of the vagina
Usually accompanied by an ileal conduit (redirection of the urine so it drains into a bag on the abdomen) or reconstruction

197
Q

What are the risk factors for renal cell carcinoma?

A

Smoking
Obesity
Dialysis

95% of upper urinary tract tumours (increasing)
30% metastases on presentation

198
Q

How might renal cell carcinoma spread?

A

Perinephric spread
Lymph node metastases
IVC spread to right atrium

199
Q

What is the treatment for localise RCC?

A

Established:

  • Surveillance
  • Radical nephrectomy (removal of kidney, adrenal, surrounding fat, upper ureter?
  • Partial nephretomy

Developmental - Ablation

200
Q

What is the treatment for metastatic RCC?

A

Palliative - molecular therapies targeting angiogenesis and now 1st choice, immunotherapy

Chemo- and radio-resistant

201
Q

What are the risk factors of upper tract transitional cell carcinoma?

A

Smoking
Phenacetin abuse
Balkan’s nephropathy

Only 5% of all malignancies of upper urinary tract

202
Q

What initial investigations are done to investigate uu transitional cell carcinoma?

A

Ultrasound - hydronephrosis
CT urogram - filling defect, ureteric stricture
Retrograde pyelogram
Ureteroscopy - biopsy, washings for cytology

203
Q

What is the standard treatment for upper urinary tract transitional cell carcinoma?

A

Nephro-ureterectomy

kidney, fat, ureter, cuff of bladder

204
Q

What is chronic kidney disease?

A

The irreversible and sometimes progressive loss of renal function over a period of months or years.
Renal injury causes renal tissue to be replaced by extracellular matrix in response to tissue damage

205
Q

What are the potential outcomes of chronic kidney disease?

A

In some, CKD inexorably worsens with progressive loss of renal function
Associated with substantial cardiovascular morbidity and mortality

206
Q

What are risk factors to chronic kidney disease?

A 
Immujnological - glomerulonephritis
Infection - pyelonephritis
Genetics - PCK, Alport's
Obstruction and reflux nephropathy
Hypertension
Vascular
Systemic disease - diabetes, myeloma
207
Q

Can the kidney regenerate?

A

No, heals with scarring

208
Q

What % of CKD is associated with glomerulonephritis?

A

10%

209
Q

In what groups of people is CKD more common?

A

Elderly
Ethnic minorities
Socially disadvantaged

210
Q

How is CKD classified?

A

According to GFR, staged 1-5
1 >90, kidney damage with normal or increased GFR Need other evidence of kidney damage (U/A or USS
2. 60-89 Kidney damage with mild GFR fall. Need other evidence of kidney damage
3. 30-59 Moderate fall in GFR. May have symptoms
4. 15-29. Severe fall in GFR. Symptoms
5. <15 or RRT. Established renal failure. Symptoms

211
Q

What is CKD a risk factor for?

A

Cardiovascular disease. Increased morbidity and mortality

212
Q

How can you measure renal function?

A 
Serum creatinine (approximate to GFR but poor) Normal range 80-120 micromol/l
GFR - inulin clearance or Cr EDTA clearance or Iohexol clearance or Creatinine clearance (24 hr urine - poor compliance)
Modified MDRD - estimate GFR taking into account serum creatinine, age, gender, ethnicity (muscle bulk). Mandated in the UK by NSF.
213
Q

What is the creatinine concentration determined by?

A

Renal function - excretes it

Muscle mass - produces it (age, sex and race affect muscle mass)

214
Q

What is eGFR accurate for?

A

Adults
White/black ethnicity (not asian)
Defines chronic kidney disease and is not useful in acute renal failure

215
Q

What is the intention of investigations of CKD?

A 
Define degree of renal impairment 
Defince cause of renal impairment
Provide patient with diagnosis and prognosis
Identify complications of uraemia
Plan long term treatment
216
Q

What can be assessed to determine the cause of CKD?

A

Auto antibody screen
Complemetn
Immunoglobin
ANCA
CRP SPEP/UPEP
Imaging - USS (size, hydronephrosis - dilation), CT, MRI
Biopsy if normal size and cause not obvious

217
Q

What is a nephrostomy?

A

Tubing system to redirect and drain kidney in hydronephrosis

218
Q

What are the complications of CKD?

A

Anaemia

Metabolic bone disease

219
Q

How does CKD cause anaemia?

A

Decreased erythopoietin production
Resistance to erythropoietin
Decreased RBC survival
Blood loss

220
Q

What is metabolic bone disease?

A

Decreased GFR -> increased phosphate -> decreased calcium -> increased PTH -> secondary hyperparathyroidism -> osteitis fribrosa cystica
Decreased GFR -> Decreased active vit D -> osteomalacia and exacerbates increase of PTH…

221
Q

How can CKD be prevented or progression delayed?

A 
Lifestyle -Stop smoking, lose weight, exercise
Treat diabetes
Treat blood pressure
ACE inhibitors/ARBs
Lipid lowering
222
Q

When is renal replacement therapy required?

A

When native renal function declines to a level that no longer adequates health. Usually 8% renal function
Dialysis/replacement

223
Q

What are the indications that dialysis is required?

A 
Uraemic symptoms
Acidosis
Pericarditis
Fluid overload
Hyperkalaemia
224
Q

What are the 2 types of dialysis?

A 
Haemoidialysis (hospital or home
Peritoneal dialysis (home)
225
Q

Where do renal transplants come from?

A

Living relative

Deceased

226
Q

What does haemodialysis require?

A 
HD machine
Artificial kidney
Hightly purified water
Vascular access - 
Anti-coagulation
Logistics - purpose built facility, trained staff, transport arrangements
Approx 4 hrs of treatment 3 days a week
227
Q

How are blood vessels modified to to accommodate for repeated cannulation?

A

AV fistula. Join cephalic vein to radial artery, cephalic vein takes more blood and walls become more muscular and substantial

228
Q

What are the advantages and disadvantages of haemodialysis?

A

Advantage - Effective, 4/7 days free from treatment, dialysis dose easily prescribed
Disadvamtages - Fluid/diet restrictions, limits holidays, Access problems, CVS instability, High capital costs, generally hospital based

229
Q

What does peritoneal dialysis require?

A

Peritoneal membrane
Peritoneal blood flow
Peritoneal dialysis fluid

230
Q

What are the advantages of peritoneal dialysis?

A

Advantages: low tech, home technique, easily learned, allows mobility, cvs stability, better for elderly and diabetics
Disadvantages: Frequent exchanges, no long term survivors, frequent treatment failures, peritonitis, limited dialysis dose range, high revenue costs

231
Q

Who is considered for renal transplant?

A

All patients with progressive CKD or end-stage renal failure should be considered

232
Q

What are the sources of renal transplantation?

A

Deceased donor
Living relative
Living emotionally related
Altruistic

233
Q

What are the advantages and disadvantages of renal transplant?

A

Advantages: Restore near normal renal function, allows mobility and rehabilitation, improved survival, good long term results, cheaper dialysis
Disadvantages: Not all are suitable, limited donor supply, operative morbidity and mortality, life long immunosuppression, still left with progressive CKD

Semester 3 (19 decks)

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