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MBChB - year 2 > Week 4 RNU Lectures > Flashcards

Week 4 RNU Lectures Flashcards

1
Q

What holds the bladder firmly at the bladder neck?

A

The puboprostatic or pubovesicle ligaments

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2
Q

What is the normal capacity of the bladder?

A

400-500ml

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3
Q

What type of epithelium is in the bladder?

A

transitional

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4
Q

What are the layers of the detrusor muscle?

A

Three smooth muscle layers (longitudinal, circular and spiral)

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5
Q

What are the layers of the bladder wall?

out in

A

Adventitia
Detrusor muscle
submucosa
mucosa - lamina propria + transitional epithelium

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6
Q

What is the venous drainage of the bladder?

A

The bladder is surrounded by a plexus of veins that ultimately drains into the internal iliac veins

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7
Q

What is the parasympathetic innervation of the bladder?

A

P=pee

  • derived from the pelvic splanchnic nerves (S2-4)
  • Motor to detrusor and inhibitory to internal sphincter
  • When fibres are stretched the bladder contracts, the internal sphincter relaxes and urine passes
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8
Q

What is the sympathetic innervation to the bladder?

A

S=storage

  • derived from T11-L2
  • transmits sensations of pain, touch and temperature
  • relaxes detrusor and contracts internal sphincter
  • bladder fills up
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9
Q

What can cause injury to the bladder?

A
  • Blunt lower abdominal trauma when bladder fully distended
  • RTA and seat belt injury
  • TURBT
  • Intravesical pressure acutely elevated and bladder perforates at weakest point- DOME
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10
Q

What are the 2 main types of receptor in the bladder?

A

Cholinergic (muscarinic) and adrenergic

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11
Q

What are the muscarinic subtypes in the bladder and where are they?

A

M1-M3 in the bladder smooth muscle

M2 is 80% of the receptors but functionally M3 is most important

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12
Q

What do M3 receptors do?

A

Mediate bladder contraction

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13
Q

What are the adrenergic subtypes of receptor?

A

B1 and B2

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14
Q

What is the bladder base made up of?

A

Trigone and bladder neck

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15
Q

What is the structure of the bladder base?

A

2 distinct layers of smooth muscle:

  • superior thin layer of longitudinal alpha-adrenergic smooth muscle contiguous with ureters
  • deep layer of smooth muscle merges with detrusor
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16
Q

What is the pre-prostatic sphincter?

A

A circumferential collar of alpha-adrenergic smooth muscle surrounding bladder neck.

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17
Q

What is the predominant receptor subtype in the pre-prostatic sphincter?

A

Alpha 1A

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18
Q

What is the structure of the rhabdosphincter?

A

Small fibres, high numbers of mitochondria, packed with lipid droplets

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19
Q

What is the function of the rhabdosphincter?

A

Likely to be a major component in maintaining continence:

  • Somatic innervation – S2/3 Onuf’s nucleus via pelvic nerves
  • Cholinergic nicotinic receptors
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20
Q

What is the structure of the urethral sphincter?

A

Circular striated muscle horseshoe (rhabdosphincter) around inner longitudinal smooth muscle (internal urethral sphincter)

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21
Q

How is continence maintained?

A
  • Alpha-blockade (sympathetic smooth muscle) reduce urethral sphincter pressure by only approx 30%
  • Therefore continence likely to result from a combination of intrinsic striated muscle tone and sympathetic induced smooth muscle tone.
  • Parasympathetic system has NO role in maintaining EUS tone
  • Parasympathetic stimulation acts to inhibit sympathetic induced tone, and to cause relaxation of urethral smooth muscle, probably by release of NO, an inhibitory neurotransmitter
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22
Q

How is pain in the bladder transmitted?

A

Travels in the pelvic nerve to the dorsal horn of S2/3/4

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23
Q

How is pain and distension from the trigone transmitted?

A

Travels with the hypogastric nerve to T10-L2

24
Q

What are the two most commonly used classifications for neurological conditions affecting bladder function?

A
  1. Location of defect
    - sacral or Infrasacral
    - Suprasacral
    - Pontine or suprapontine
  2. Functional outcome
    - Detrusor (overactive, normoactive or underactive)
    - Sphincter (overactive, normoactive or underactive)
25
Q

What is expected in the urodynamic findings of a patient with a suprapontine lesion?

A

detrusor hyperreflexia and synergic striated sphincter

26
Q

What is expected in the clinical examination of a patient with a spinal/Suprasacral lesion?

A
  • Muscle spasm, brisk reflexes
  • positive digital anal reflex
  • Positive bulbocavernosus reflex
27
Q

What is the bulbocavernosus reflex?

A

elicited by squeezing the penile glans or the clitoris and feeling for an involuntary contraction of the anus

28
Q

What is expected in the urodynamic findings of a patient with a spinal/Suprasacral lesion?

A
  • Detrusor hyperreflexia
  • Detrusor sphincter dyssynergia
  • normal compliance
29
Q

What is expected in the urodynamic findings of a patient with a conus or Infrasacral lesion?

A
  • Areflexic or underactive detrusor
  • low compliance with open bladder neck
  • Urethral sphincter incompetence
30
Q

What is expected in the clinical examination of a patient with a conus or Infrasacral lesion?

A
  • Negative digital anal reflex

- Negative bulbocavernosus reflex

31
Q

What are common causes of suprapontine neurogenic bladder?

A
  • Dementia
  • Parkinson’s disease
  • Urge and urge incontinence exacerbated by poor mobility
  • CVA
32
Q

What happens in suprapontine lesions?

A

Overactive bladder with intact sphincter behaviour

- failure of higher centre control leads to frequency, nocturia, urgency and urge incontinence

33
Q

What happens in Suprasacral lesions?

A
  • Preserved spinal reflex arch; disruption of descending inhibition and pontine co- ordination; typically bladder overactivity with detrusor-sphincter dyssynergia (DSD)
34
Q

What happens in Infrasacral lesions?

A

characterised by bladder acontractility and paralysis of urethral sphincter.

35
Q

What is Obstructive uropathy?

A

High renal pressure, low blood flow, impaired homeostasis and excretion

36
Q

What is obstructive nephropathy?

A

Damage to renal parenchyma resulting from obstruction to flow of urine

37
Q

What is obstructive uropathy commonly associated with?

A

High pressure chronic retention (HPCR)

38
Q

What is HPCR?

A

maintenance of voiding, with a bladder volume over 800mls and an intra-vesical pressure above 30cm H2O, usually accompanied by hydronephrosis

39
Q

What are the signs/symptoms of HPCR?

A
  • Tense painless bladder
  • Maintenance of micturition
  • Renal impairment
  • Bilateral hydroureteronephrosis
  • May also have-overflow incontinence, nocturnal enuresis and hypertension3 (50%)
  • Peripheral oedema and congestive cardiac failure (20%)
40
Q

What are the 3 stages of prostatism?

A
  1. Prostatic hypertrophy causes increasing outlet resistance causes bladder muscle hypertrophy- trabeculation
  2. As this progresses sacculation and diverticulum formation occurs and ureters dilate
  3. Bladder becomes decompensated – flaccid, large and over distended NB overflow incontinence
41
Q

What are the 2 components of BPO?

A
  • Dynamic: α1-adrenoceptor- smooth muscle contraction, approx. 40% area density of hyperplastic prostate
  • Static: volume effect of BPE
42
Q

What happens to the bladder wall in HPCR?

A
  • Thick, detrusor hypertrophy
  • Histology- smooth muscle bundles degenerate into collagen*
  • obstructs Vesico-ureteric junction (VUJ)- possibly more when bladder empties
  • So not transmission of high pressure to upper tracts i.e. reflux but obstruction of VUJ
43
Q

Where is most of the total body potassium found?

A

In muscle

44
Q

What is the average UK intake of potassium?

A

80mmol/d

45
Q

What levels of potassium intake can the body cope with (if it has normal renal function)?

A

20-500mmol/d

46
Q

Where does the majority of work in the kidney take place?

A

The cortex

47
Q

What controls glomerular filtration rate?

A
  • blood flow
  • Angiotensin II - efferent arteriole vasoconstriction
  • Myogenic control
  • SNS - direct vasoconstriction
  • Reduced blood volume - baroreceptor - SNS/renin - ADH/AgII - increased sodium reabsorption ‘distal sensing’
48
Q

What happens to blood supply to the kidney when someone is in shock?

A

Blood supply stops because the afferent supply to the kidney is controlled by the sympathetic nervous system

49
Q

How is the concentration of a solute measured in the body?

A

Osmolarity = [osmole]/unit volume(l)

Osmolality = [osmole] / unit mass (kg)

50
Q

What is the only hormone involved in the proximal convoluted tubule?

A

Angiotensin II which partially controls sodium

51
Q

What are the rules for the loop of Henle?

A
  1. Thick ascending limb is impermeable to water, but actively transports sodium, potassium and chloride
  2. Thick ascending limb provides the concentration gradient to promote water reabsorption from the thin DLH
  3. Thin descending limb is freely permeable to salt and water
  4. Vasa recta doesn’t wash away the gradient by using counter current exchange
52
Q

What do thiazide diuretics result in?

A

No Na+ reabsorption

53
Q

How is urea produced?

A

it is a by-product of amino acid metabolism in the liver

54
Q

Where is urea reabsorbed?

A

The inner medullary collecting ducts (passively)

55
Q

How is creatinine produced?

A

breakdown product of creatinine phosphate, muscle metabolism

56
Q

What happens to drugs at bowman’s capsule?

A

Filtration of all drugs of low molecular weight

MBChB - year 2 (25 decks)

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