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YEAR 2 SEMESTER 2 > renology and urology - wk 4 > Flashcards

renology and urology - wk 4 Flashcards

1
Q

describe the structure and function of the bladder wall

A
  • Apical membrane with tight junctions
  • Tight junctions important wall in cellular signalling
  • As bladder fills it stretches and tight junctions send signals to further centres
  • Allow control of bladder – voiding
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2
Q

papillary bladder tumour - type of cancer and symptoms

A
  • Papillary bladder tumour – type of urothelial cell cancer (transitional cell cancer)
  • Leads to painless visible haematuria (blood in urine)
  • Bladder discomfort
  • Urgency and frequency to pass urine
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3
Q

what are the 4 layers of the bladder wall

A

Urothelium
- Multi-layered epithelium
- Apical (umbrella cells)
- Functions – barrier, afferent signalling
Lamina Propria
- ‘functional centre’ coordinating urothelium and detrusor
- Blood vessels, nerve fibres, myofibroblasts
Detrusor muscle stroma
- Smooth muscle arranged in bundles
- Functional syncytium
- Each detrusor cell – 600 microns long by 5 microns
- Stroma – collagen and elastin
- Innervation of muscle – postganglionic parasymp
Adventitia/ Serosa

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4
Q

what are the normal bladder functions - (remember to talk about its function as a barrier)

A 
Compliant reservoir 
-	For urine storage
Barrier function (GAG layer, tight junctions)
-	Passive passage of urea, Na, K
-	Resists water passage but not truly waterproof
-	Damage to urothelium – role of disease
Volitional Voiding
-	(muscular function)
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5
Q

describe the bladders function as a compliant urine storage

A
  • Bladder pressure remains constant despite increase in volume
  • Bladder is highly compliant
  • Visco-elastic properties (elastin/ collagen – detrusor relaxation)
  • Without change in tension
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6
Q

how does the bladder respond to filling

A

Bladder Filling – sensors detect increase in wall tension

  • Afferent neurons to dorsal horn of sacral spinal cord
  • Sensory/ real time data on bladder state relayed to brainstem and higher centres
  • Higher centres control the bladder muscle further
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7
Q

explain why and how volitional micturition/ voiding happens

A
  • Spino-bulbar reflex
  • Modulation by pontine micturition centre (Barrington’s nucleus)
  • Onuf’s nucleus in intermediolateral S2, 3, 4

Fullness at 250ml – uncomfortable at 500ml (detrusor contractions)
- Coordination of
o Detrusor muscle
o Urethral relaxation
- Relaxation of external urethral sphincter –
o Urine enters posterior urethra

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8
Q

describe higher control of voiding

A
  • Involves prefrontal, hypothalamic, thalamic, cerebellar areas
  • Most important is the pons – pontine level
    o PMC – pontine micturition centre
    o This takes afferent signals from sacral level up signal cord
    o Processed by PMC
    o Fires down efferent signals back to bladder – sphincter muscles
    o Leading to voiding
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9
Q

whats the positive feedback loop involved in micturition

A

During voiding itself the detrusor muscle is firing a positive feedback loop

  • As detrusor muscle contracts
  • Wall tension in detrusor muscle rises
  • Afferent signals to PMC to be processed
  • Efferent signals sent out to increase detrusor contraction
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10
Q

what muscles and nerves are involved in voiding

A
  • Voiding achieved by detrusor muscle contraction and sphincter muscle relaxation
    o Via the pelvic nerves, pudendal nerves and Parasympathetic motor nerves
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11
Q

what neurotransmitters are involved in bladder control

A

Excitatory – cholinergic (Ach)
- Role of nitric oxide in relaxation of bladder neck/ EUS (external urethral sphincter)

Inhibitory - GABA and glycine

  • Bladder activity subject to facilitation and inhibition (higher centres and local reflexes)
  • Facilitation = contraction of detrusor and relaxation of sphincter when bladder less than full eg anxiety states
  • Inhibition = allows postponement of voiding
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12
Q

how do different spinal cord injuries effect bladder control

A

SPINAL CORD INJURY

  • Loss of central inhibition
  • Typically, reflex voiding (pelvic parasympathetic nerves)
  • Involves pudendal nerves

Suprapontine lesion

  • Detrusor overactivity
  • Urgency and frequency

Spinal (infrapontine – suprasacral) lesion

  • Detrusor overactivity, detrusor-sphincter dyssynergia
  • Urgency and dysfunctional voiding
  • Difficulty voiding
  • Don’t empty bladder to depletion

Sacral/ infrasacral lesion

  • Poor intermittent urinary flow
  • Hypocontractile or acontractile detrusor (underreactive)
  • Urinary incompetence
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13
Q

what’s a normal voiding pattern

A
  • When bladder contains 300mls (and its socially convenient) VOIDING is initiated
  • Normal voiding pattern – 300-400mls per void, 4-5 per day (<7) depending on input
  • No urgency or incontinence
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14
Q

what does a frequency chart record

A
  • Used to figure out how troubling the patient’s urinary frequency is
  • Collected by patient
  • Informative
    o Frequency
    o Functional capacity
    o Nocturia
  • Doesn’t give info on digested fluids by the patient
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15
Q

what does a bladder diary record

A

(INPUT AND OUTPUT CHART) – the ideal diary chart
- Collected by patient
- 3 consecutive days
- NB – monitors input as well as output
- Type of fluid eg water, caffeine, alcohol noted
- Most informative chart
o Frequency
o Functional capacity
o Nocturia
o Also input diary detects hyperhydration / excessive intake, effects of caffeine, EtOH, diurnal ingestion patterns and binges
o “Wet” (UI) episodes

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16
Q

storage symptoms

A

Storage symptoms are characterised by an altered bladder sensation

  • Urgency
  • Frequency
  • Nocturia
  • UI – urinary incontinence
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17
Q

voiding symptoms

A
  • Hesitancy
  • Poor flow
  • Intermittency
  • Terminal dribbling
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18
Q

what can increase urinary or decrease storage capacity (leading to freqeuncy)

A
  • Polyuria – consider DM/DI, or excess fluid intake
  • Decreased bladder capacity – reduced compliance, reduced functional capacity, neurogenic bladder, irritation (bladder stones/ tumour)
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19
Q

define nocturia and explain whos at risk and why

A
  • Normal <2x night
  • Ageing bladder, bladder outlet obstruction BOO, decreased compliance, dietary habits
  • Effect of ageing – renal conc. Ability decreases with age
  • Increased renal blood flow at night (lying down) leads to increased urine production
  • Risk of falls and injury
  • Patients with ankle oedema (heart problems) renal system reabsorbs fluid at night = nocturia
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20
Q

define nocturnal polyuria

A
  • Production of more than 1/3rd of 24-hour urine output between midnight and 8am
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21
Q

what are the 2 general causes of poor flow, hesitancy and dribbling

A
  • Decreased force of micturition usually secondary to bladder output destruction (BOO, urethral stricture) – aka ‘plumbing problem”
  • May also occur with underactive/ hypocontractile bladder (eg SC injury) – aka ‘pump problem’
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22
Q

define hesitancy, intermittency, post-void dribbling and straining

A
  • Hesitancy – delay in start of micturition
  • Intermittency – involuntary start-stop; prostatic enlargement
  • post-void dribbling ¬– release of small amount of urine after micturition
    o due to release of urine retained in bulbar/ prostatic urethra
  • Straining – use of abdominal muscles to void (Valsalva only normally required at end of voiding)
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23
Q

define incontinence

A

‘involuntary loss of urine that is a social or hygienic problem and is objectively demonstrable’

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24
Q

what are the 2 types of incontinence and give a brief description

A 
Urge incontinence (UUI)
-	Involuntary loss of urine associated with strong desire to void (detrusor contraction)
Stress incontinence (SUI)
-	Involuntary loss of urine when intra-abdominal pressure rises without detrusor contraction eg with coughing, sneezing, laughing straining, exerting
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25
Q

how do we assess bladder symptoms

A

Take history
- F/ V chart or bladder diary
- Examination
o Rectal examination in men – expect prostate, and rectal turn (to check for spinal injury)

Urinalysis

Special Investigations

  • IPSS (international prostate symptom score)
  • Flow rate and PVR (post-void residual vol)
  • Urodynamics
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26
Q

international prostate symptom score (IPSS), what does it consist of and what do the results imply

A 
7 questions - Patient rates each symptoms out of 5
-	Frequency
-	Nocturia
-       Urgency
-	Weak urinary stream
-	Hesitancy
-	Intermittency
-	Incomplete bladder emptying
Plus quality of life (QoL)/ bother score question, 0 = delighted, 6 = terrible
Score 
-	0-7/ 35 > mild symptoms
-	8-19/ 35 > moderate symptoms
-	20-35/35 severe symptoms
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27
Q

UroFlowMeter - what does it measure/ assess

A
  • Asses voided volume, maximal urinary flow rate
  • Bladder scan – assess residual volume
    o Over 200ml significant
  • Voiding time
    o Prolonged voiding time = bladder output obstruction
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28
Q

urodynamic assessment - why, how and on who do you carry this out

A
  • Determine underlying cause
  • Indicated in patients with complex voiding patterns, suspected neurological abnormalities, young patients with severe symptoms
  • Involves placement of pressure transducers in
    o Bladder and rectum
  • Pressure from each of these measured during filling and voiding
  • Patient asked to cough periodically
  • Subtracting rectal (abdominal) pressure from bladder = detrusor activity
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29
Q

what is measured in a urodynamic assessment and how

A

urethral catheter is placed in the patient
o within this is the pressure transducer
o measure intravesical pressure

  • Also a pressure transducer in the rectum to measure the abdominal pressure
  • Intravesical pressure – abdominal pressure = detrusor pressure
  • During filling phase constant rate of fluid infused into bladder – usually saline
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30
Q

what is seen in a normal urodynamic trace

A

during filling phase

  • detrusor pressure kept low
  • when patient coughs no urinary flow or increase in detrusor pressure
  • no spontaneous rises in detrusor pressure

during voiding phase

  • rise in intravesical and detrusor pressure
  • normal urinary flow
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31
Q

what is seen in a urodynamic trace of someone with urinary incontinence - via detrusor overactivity

A

during filling phase

  • spontaneous rises in detrusor pressure = increase urinary flow
  • when patient coughs there’s no rise in detrusor pressure

during voiding phase
- rise in intravesical and detrusor pressure as normal leading to urinary flow (no evidence of blockage)

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32
Q

what is seen in a urodynamic trace of someone with stress incontinence

A

In filling phase

  • when patient coughs the urinary flow increases
  • detrusor pressure is constant ie compliance is normal

voiding phase is normal

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33
Q

what is seen in a urodynamic trace of someone with outflow obstruction

A

in filling phase
- no urinary leakage

During voiding phase

  • flow of urine is quite low
  • large rise in detrusor pressure
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34
Q

symptoms of outflow obstruction of the bladder - why is the “bladder and unreliable witness”

A
  • ‘the bladder is an unreliable witness’ because symptoms that patients describe do not always determine the main underlying problems
    o The storage symptoms may come first (bother the patients the most)
    o Then voiding (obstructive) symptoms come later
    o Then decompensation of detrusor
     Residual urine, chronic retention
     Bladder failure
     Renal failure
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35
Q

management of the 3 main low urinary tract syndromes

A

Over-active bladder
- Lifestyle (cut back on diuretics), anti-muscarinics (solifenacin, fesoterodine, oxybutynin), selective beta-3 adrenoreceptor agonist (mirabegron), intradetrusor botox

Stress incontinence
- Pelvic floor exercises, weight loss, surgery (autologous rectus abdominis sling, artificial sphincter)

Bladder outlet obstruction
- Medical therapies – alpha-blockers

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36
Q

what are the 3 main blood markers in advanced kidney disease

A
  • High creatinine
  • High potassium
  • Low bicarbonate – acidosis
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37
Q

what are the symptoms of advanced kidney disease

A
  • Tired
  • Itchy skin
  • Short of breath – anaemic
  • Cramps – low calcium
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38
Q

whats the definition of CKD

A

GFR of less than 60ml/min for >90 days/ 3 months

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39
Q

what are some important causes of CKD

A
  • Diabetes/ hypertension/ glomerulonephritis/ cystic kidney disease/ renovascular disease
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40
Q

how do we estimate renal function

A
  • Normal GFR – 125 ml/min/1.73m^2
  • Serum creatinine clearance (24 hr urine collection)
    o May be affected by age/ muscle mass/ drugs
    o Urea and creatinine clearance more accurate
  • Isotope GFRs
    o Expensive and time consuming
  • Formulae
    o For estimated GFR (MDRD) or Creatinine clearance (cockcoft and gault) – based on creatinine
    (Urine concentration x volume) / plasma concentration for CREATININE
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41
Q

why is serum creatinine not a good marker of renal function

A
  • Older people have decreased muscle mass

o So creatinine can be normal even in advanced disease

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42
Q

the stages of CKD - what are the factors that must be met for stage 1 and 2, at what stage would you start dialysis/ transplantation

A

For stage 1 and 2 you must have another factor
- Biopsy proven/ radiology proven kidney disease
- Presence of polycystic kidney disease
Stage 4 – plan for dialysis
Stage 5 – plan for dialysis / transplantation

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43
Q

how common in CKD

A
  • 6.2% population have CKD 3

- Given elderly population have more CKD, up to >25% of elderly pts may be expected to have stage 3 ckd 3 or worse

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44
Q

what are prevention strategies for CKD

A
  • Control blood pressure (RAS inhibititors)
  • Reduce proteinuria (RAS inhibition)
  • If diabetes, optimise glycaemic control
  • SGLT2 inhibitors (diabetes)
    o CREDENCE trial – Canagliflozin
     Good outcomes for renal and CV
    o Dapagliflozin
    o Empagliflozin
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45
Q

proteinuria as a cause of CKD

A
  • In glomerulus
  • All have protein in filtrate which is taken up into tubular cell and taken up into peritubular capillaries and recycled
  • If we have lots of protein in blood (eg diabetes) this system is overloaded
  • Leading to free radicals and cell dies
  • In effort to clear away dead glomerulus fibroblasts and macrophages come and get rid of dead cell
    o This allows for regeneration of new cell
    o But leaves fibrosis behind
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46
Q

what drug is useful in proteinuria and why

A

ACE inhibitors are useful…

  • Dilate the efferent arteriole
  • Reduces glomerular pressure
  • Reduces amount of proteinuria
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47
Q

how to safely prescribe drugs in CKD, what drugs to avoid

A

Avoid potential toxins

  • NSAIDs/ contrast/ gentamicin
  • Phosphate enemas
Drug dosing
-	Many drugs need to be given at a lower dose in patients with CKD
o	Especially chemotherapy/ antibiotics
-	If in doubt check BNF app
-	Rem - >25% of elderly pts may have CKD
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48
Q

complications of CKD and target BP goals

A

Cause/ consequence
- Causes left ventricular hypertrophy/ stroke/ end-organ damage – eyes/ kidneys

BP treatment goals

  • 130/80
  • 125/75
49
Q

potassium in CKD

A 
-	Important to monitor in all CKD
o	Becomes common as GFR declines <25
o	Related to distal sodium delivery (DND low, with low GFR)
-	Dietary advice re High K foods
-	Potassium binder
o	Patiromer/ sodium zirconium
50
Q

acidosis in CKD

A
  • Much acidosis in CRF is due to animal protein in food
    o Inability to acidify urine in CKD
    o Phosphate/ sulphates/ other anions – v late
  • Aim to keep serum HCO2 >22
  • Replace with NaHCO3 >22
  • Replace with NaHCO3/ sodium bicarbonate
    o JASN, 2009
    o But beware fluid overload
51
Q

anaemia in CKD

A
  • Hb <12 in males/ <11 in females
    o Generally monochromic normocytic anaemia
  • Decreased response of EPO to a hypoxic stimulation (kidneys) and…
    o Decreased red cell survival
    o Iron deficiency
    o Blood loss – dialysis/ blood samples/ GI
    o Aluminium/ hyper PTH/B12 + folate deficiency
52
Q

erythropoietin (Epo) replacement therapy

A
  • All pts with Hb<105 and adequate iron stores should be on Epo
    o Better quality of life/ less dyspnoea/ reduced left ventricular hypertrophy
  • Target Hb 100-120
    o S/ E – hypertension/ thrombosis
  • If poor response to EPO
    o Check iron stores/ CPR/ B12 + folate/ PTH/ aluminium/ ?malnutrition/ malignancy
53
Q

renal osteodystrophy > what are the 2 subdivisions

A 
-	High turnover bone disease
o	Secondary hyperparathyroidism
-	Low turnover bone disease
o	Osteomalacia
o	Adynamic bone disease
o	Aluminium bone disease
54
Q

why do you get renal osteodystrophy in CKD

A
  • Kidney responsible for formation of vitamin D
  • Vit D levels drop if kidneys not working
  • Without vit D can’t absorb as much calcium from gut – hypocalcaemia
  • This can cause rickets and osteomalacia – aka softening of the boning
55
Q

Whats the bodys response to low calcium

A
  • PTH increases to try to normalise Ca levels, leading to …
    1- increases absorption of calcium phosphate from gut and bone
    o Cause secondary hyperthyroidism, osteitis fibrosa
    o = brown tumours in bone, erosion of bone etc

2- decreases Po4/phosphate levels
o Phosphate needs to be excreted by kidney
o If kidneys not working well = hyperphosphatemia

56
Q

what ckd patients are affected by the following conditions -osteoporosis, adynamic bone disease, aluminium bone disease

A 
Osteoporosis
-	In patients who are older/ immobile
Adynamic bone disease
-	When we give vit D to patients it has an exaggerated response…
-	Drops PTH level
-	So can’t use vit D in these patients
Aluminium bone disease
-	High aluminium in water supply
-	Seams of aluminium lay down in bone = weak and increase fractures
57
Q

treatment of renal osteodystrophy

A 
-	Phosphate restriction 
o	Diet
o	Binders – calcium or non-Ca binders
-	Vitamin D therapy
o	Increases Ca/ decreases PO4
-	Monitor PTH 6/12ly
o	Keep 2-3x normal
-	Parathyroidectomy may be required
58
Q

what are the consequences of hyperphosphataemia

A 
-	Vessel calcification – in medial layer of vessels
o	Non-compliant vessels
o	Systolic hypertensin
o	Diastolic hypotension
-	Calciphylaxis > bad ulcers 
-	Increases BP – cardiovascular disease
59
Q

malnutrition in CKD

A
  • Malnutrition is common in CKD
    o Decreased protein intake to decrease phosphate
    o Decreased appetite
    o Low albumin 0 related inflammation?
  • Malnourished patients do worse on dialysis
  • MDRD study
    o No benefit of v low protein diet in ESRD
    o But diet with 0.6-0.8g/kg a day advised
60
Q

who should be referred to the renal clinic

A
  • Any patient with rapid increase in creatinine/ hypertension
  • Stage 3 CKD with hypertension/ proteinuria/ haematuria/ rising creatinine
  • Any stage 4/5 CKD who is suitable for treatment (If old and frail it’s harder)
  • Late referral patients do considerably worse
    o Anaemia/ renal bone disease/ dialysis access
61
Q

what are the 2 main types of dialysis and describe each

A

Haemodialysis
o Create fistula in arm to join up artery to vein
o Take blood out to be cleaned by machine
o Put back into vessel
2-3 days

Peritoneal dialysis
o Potential space between gut and anterior abdominal wall
o Put clean fluid in this space
o Patient goes about normal life waster products go into fluid
o Fluid is drained out and new fluid put in
24/7

62
Q

transplantation for CKD

A
  • Cadaveric graft and plug it in
  • Gold standard treatment
  • Need to take drugs to allow immunosuppression
63
Q

Conservative care of CKD

A
  • If patient choices not to have dialysis
  • Usually old and frail patients
  • Involves treating symptoms
64
Q

when and how to start dialysis

A

When to start
- Creatinine clearance 9-14

CAPD – for peritoneal dialysis

  • Catheter insertion into peritoneal membrane
  • Training with nursing dialysis team

AV fistula – haemodialysis

  • Preservation of vessels in non-dominant arm
  • Needs 3-4 months maturation before use
65
Q

whats the normal body sodium levels and what are the levels in hyponatraemia

A
  • Normal serum sodium – 135-145 mmol/l

- Hyponatraemia – below 135

66
Q

total body water in men and women

A
  • Men – 60% water – 42 litres

- Women – 55% water – 38 litres

67
Q

what are the compartments into which fluid can spread in the body

A
  • Intracellular – 30 litres
  • Interstitial space – 9 litres
    o Bathes the cells
  • Vascular – 3 litres (kidney, guts, lungs, skin)
    o Can track gut and kidney water loss, hard to track lungs and skin
    o These “insensible losses” go up in hospitals
68
Q

what are 2 important salts in the compartments

A
  • Potassium and sodium
    o K intracellular
    o Na extracellular
  • Water moves to keep each compartment at same concentration
69
Q

what causes water to move between compartments

A 
Out
-	Int. hydrostatic pressure
-	Ext. osmotic pressure
In
-	Ext. hydrostatic pressure
-	Int. osmotic pressure
70
Q

what would hypothetically happen if we added sodium to the extracellular compartment

A
  • (murder)
  • By adding salt, you are massively raising osmolarity in this compartment
    o Sodium can’t get into the intracellular compartment (as this is where K is)
    o So sodium is entirely in the extracellular compartment
  • Since water can move freely you deplete the cellular reservoir to over hydrate the extracellular reservoir
71
Q

what would happen hypothetically if we added water to the extracellular compartment

A
  • Add water to extracellular compartment eg fluid overload
  • This would firstly expand the vascular space
  • Then water would flow into the interstitial space
  • Flow into the cellular space as well
    o As your diluting each of the above space
    o Increased the hydrostatic pressure bc you’ve increased the volume
    o So water completely distributes across these 3 compartments
    o This dilutes the sodium down
72
Q

what ultimately causes death in hyponatraemia

A
  • Cerebral oedema occurs
  • Confusion
  • Expansion of brain within intracranial space can = death
  • this is due to water moving into the hypertonic cellular space as the extracellular space has low levels of sodium
73
Q

how does total water volume effect sodium

A
  • Most people are normal, with 55-60% total body water, they are…
    o Euvolaemic/ normovolaemic
  • Some people are volume deplete; they are…
    o Hypovolaemic
    aka dehydration
  • And some people can be volume overloaded, they are
    o hypervolaemic
74
Q

what are the 3 types of hyponatraemia

A
  • norvolaemic hypotraemia
  • hypovolaemic hyponatraemia
  • hypercolaemic hyponatraemia
75
Q

compartment sizes in clinical practice - what does increase/ decrease in compartments lead to

A

Cellular compartment ~2.5x size of extracellular compartment

  • if you deplete or expand compartments but ratio remains same = look normal
  • if you deplete the extracellular department only = hypovolaemic
  • if you expand the extracellular department only = hypervolemic
76
Q

hypovolaemia clinical signs

A
  • postural hypertension (dizzy, fall over when stand up eg in morning)
  • tachycardia (because blood volume decreased)
  • absence of jugular venous pulse @ 45 degrees (if you can’t see it when they’re lying flat – very bad)
  • reduced skin turgor / dry mucosae (volume depleted = reduced skin turgor)
  • supine hypotension (low blood pressure while lying flat)
  • oliguria (pass smaller vol. of urine than they should – not enough fluid)
  • organ failure
77
Q

hypervolaemia - clinical signs

A
  • hypertension
  • tachycardia
  • raised jugular venous pulse @ 45 degrees
  • gallop rhythm (3rd heart sound between the 2 normal ones)
  • peripheral and pulmonary oedema
  • ‘third space gains’
    o Spaces like peritoneal spaces, fluid spaces, joint spaces
  • Organ failure
78
Q

how can gastritis/ diarrhoea cause hypovolaemic hyponatraemia

A
  • Salt rich-diarrhoea
    o Because lost some of small bowel so can’t absorb the solutes normally
    o Water loss cannot compensate for Na+ loss (more salt than water lost)
    o Sodium cannot become concentrated back up again
    o Hyponatraemia ensues
79
Q

hypovolaemic hyponatraemia - description and associated diseases

A
  • Excessive sodium losses, water losses are insufficient to concentrate sodium back up
  • Depends on volume of water lost and concentration of sodium therein
Clinical scenario
Diseases-
-	Haemorrhage
-	Vomiting
-	Diarrhoea
-	Burns
-	Diuretic states
-	Sequestration
-	Misc. renal diseases
-	Heat exposure
-	Addison’s disease
Iatrogenic
-	Diuretics
-	Stomas/ fistulas
-	Gastric aspiration
80
Q

euvolaemic hyponatraemia

A
  • Water being evenly distributed across all compartments
  • Hyponatraemia is dilutional
  • Common causes
    o Hypotonic intravenous fluids
    o Hypothyroidism
    o SIADH
81
Q

hypervolaemic hyponatraemia

A
  • Patients gaining lots of fluid
  • Water gains exceed sodium gains
  • 3 classic cases
    o Heart failure
    o Liver failure
    o Nephrotic syndrome
82
Q

heart failure in relation to hypervolaemic hyponatraemia

- basic signs of heart failure and how reduced cardiac output in heart failure leads to hyponatraemia

A
  • Heart enlarged
  • Base of both lungs opaque because of water
  • Top of lungs are fuller than they should be because of water

Reduced cardiac output in HF
- Reduced effective circulating volume
o If heart stunned/ attacked = cardiac output dropped
o Switches on pressure sensors
o These tell rest of the body correcting this by bringing more fluid into vascular space so heart can function better
o These sensors don’t pick up that it’s actually the hearts fault – only pick-up hypovolaemia – because sensors detect reduced organ perfusion
- Reduced organ perfusion
- Physiological correcting mechanisms kick in
- Hypovolaemia wins over tonicity
o So sodium will keep on plummeting as more fluid is brought into vascular space thereby diluting sodium
- Renin/ angiotensin/ aldosterone stimulation
- ADH stimulation

83
Q

correcting mechanism in heart failure leading to hyponatraemia

A
  • Sodium retention (aldosterone)
  • Water retention (thanks to aldosterone and ADH)
  • Hyponatraemia results from dilution
  • Fluid overload worsens LV function
    o CO actually gets worse = maladaptive
  • Hypovolaemia continues to win over hyponatraemia
  • Vicious cycle worsens
84
Q

SIADH (syndrome of inappropriate ADH secretion) - how does it cause hyponatraemia

A 
ADH is an anti-diuretic
-	ADH secretion is excessive
o	Not suppressed by reduced tonicity
o	Water reabsorption is excessive
o	(and inappropriate)
o	Sodium is diluted
o	Hyponatraemia results
-	Clinically euvolemic (both compartments expanded in same amount)
85
Q

what causes SIADH

A

Pituitary hypersecretion / direct effect
o Neurological
 Meningitis, encephalitis, head injury, stroke etc
 Aka injury to pituitary gland

Ectopic secretion
o Malignancy – because ADH-like molecules are secreted
 SCLC (small cell lung cancer), pancreas, bladder, prostate etc
 Pulmonary (non-malignant)
• TB, pneumonia etc

Potentiation of action
o Drugs eg thiazide diuretics, carbamazepine, amitriptyline

86
Q

treatment for hyponatraemia

A 
For hypovolaemia
-	Restoration of volume state
o	Blood if necessary
o	Crystalloid (0.9% saline)
-	Cessation of diuretics
-	Steroids for Addison’s
Hypervolaemia
-	Diuretics
o	Loop diuretics
	Furosemide/ bumetanide
-	Fluid restriction
-	Treatment of underlying cause 
o	Eg of heart attack
Euvolemic hyponatraemia
-	Treat underlying causes
o	Stop IV fluids
o	Thyroxine replacement
-	Fluid restriction
o	Down to 500ml/ day
-	Rarely
o	Demeclocycline
	Reduces tubular sensitivity to ADH
87
Q

what are the vasa recta and where are they found

A

vasa recta capillaries supply the renal tubule associated with each glomerulus

88
Q

what are the 3 main parts of the nephron

A
  • renal corpuscle/ bowman’s capsule containing glomerulus capillaries
    o supplied by afferent arteriole and drained by efferent arteriole
  • filtered plasma drains into a renal tubule
  • renal tubule surrounded by networks of capillaries supplied by efferent arteriole and vasa recta which returns reabsorbed fluid back into systemic circulation via renal veins
89
Q

what happens to the kidney as we age

A
  • typical GFR young healthy adult 120ml/min
  • lose half renal function by age of 80
  • rate of decline greatly accelerates by chronic conditions
    o eg hypertension, diabetes
90
Q

what are the signs of chronic renal impairment

A 
Reduced clearance of
-	urea, creatinine
-	sodium, potassium
-	phosphate
-	drugs
fluid retention
acidosis
anaemia
-	caused by development of uraemia and decrease in erythropoietin
renal bone disease\
-	caused by phosphate retention, and inability to convert precursors into active vit D
91
Q

what are the 3 categories of renal impairment

A

Pre-renal due to renal function decline due to failure to deliver sufficient blood to renal cortex

Renal causes due to direct injury to renal tissue due to intrinsic renal diseases ro damaging effects of drugs/ toxins

Post-renal causes due to obstruction of renal tract eg compression of ureter due to retroperitoneal tumour

92
Q

what drugs effect glomeruli function aka RAAS inhibitors

A

ACE inhibitors – eg ramipril, lisinopril

  • inhibit ACE so angiotensin 1 isn’t converted to angiotensin 2
  • stops constriction of afferent artery

Angiotensin receptor antagonists eg losartan, candersartan
- block effects of Ang. 2 at its receptor

93
Q

what drugs effect the proximal tubule

A

SGLT-2 inhibitors – eg canagliflozin

  • inhibit co-transporter protein that reabsorbs glucose with sodium
  • increase urinary excretion of glucose
  • indicated in type 2 diabetes

Uricosuric drugs – febuxostat, probenecid (no longer used – prevent excretion of penicillin)

  • block reabsorption of uric acids
  • used in gout
94
Q

what drugs effect the distal tubule

A

PTH analogues – synthetic PTH

  • to maintain reabsorption of calcium
  • in patients with chronic hypoparathyroidism
95
Q

what drugs effect the collecting ducts

A

Vasopression analogues – desmopressin

  • vasopressin stimulated aquaporins in collecting duct to increase uptake of water
  • used in diabetes insipidus – patients have high urinary flow and dehydration as they can’t produce vasopressin

Vasopressin inhibitors – demeclocycline, tolvaptan
- used in excessive secretion of vasopressin – in cancer or with some drugs SIADH
o this causes excess water reabsorption = hyponatraemia
- inhibits responsiveness of collecting duct cells to vasopressin
- so reduces water reabsorption

96
Q

what replacement products are used in kidney treatment

A

Epoetin’s – eg epoietin beta, darbopoietin
- used to treat anaemia in CKD
Vitamin D analogues – alfacalcidol, calcitriol
- hydroxylised derivatives of vit D as in Kidney disease kidneys can’t hydroxylase vit D well
Sodium bicarbonate
- to combat metabolic acidosis

97
Q

what are the 3 main ways drugs can adversely effect the kidneys

A

excessive fluid loses causing a reduction in extracellular volume
o reduces circulating volume
o reduces BP and tissue perfusion
o activates RAAS and SNS
o which protects perfusion of vital organs in dehydration
o in the kidney…
 short-term the afferent arteriole is constricted which increase GFR
 in progressive dehydration GFR drops and waste product removal compromised

drugs with direct effects on renal vasculature
o vasoconstriction of the afferent arteriole
o impaired influence of angiotensin on the efferent arteriole

direct toxic effects
o on tubular or interstitial cells leading to…
 acute tubular necrosis
 acute interstitial nephritis

98
Q

how do drugs cause dehydration?

A
  • stimulates SNS to cause vasoconstriction and reduce perfusion in kidney
  • this decrease amount of blood supplied to glomeruli and reduces filtration
  • this reduces GFR and volume of urine produced
  • in mild dehydration RAAS protects GFR
    o release of renin in response to NaCl and SNS
    o angiotensin 2 restricts afferent arteriole – higher GFR
99
Q

what drugs cause dehydration

A 
Diuretics
o	Loop diuretics (eg furosemide)
o	Thiazide diuretics (eg Bendroflumethiazide)
-	If these drugs are causing dehydration you get…
o	Thirst
o	Dizziness standing up
o	Increased skin turgor
o	Hypotension
o	Increased urea and creatinine

Drug-induced diarrhoea

  • Laxatives (eg senna, lactulose)
  • Proton pump inhibitors (eg omeprazole)
  • Antibiotics
  • Many others (eg digoxin, colchinine)
100
Q

what drugs alter renal perfusion

A

Drugs suppressing the renin-angiotensin system
- Angiotensin converting enzyme (ACE) inhibitors (eg ramipril)
- Angiotensin receptor antagonists (ARAs) (eg iosartan)
- Block the formation or actions of angiotensin 2
Adverse effects are particularly likely if renal function is already threatened by hypovolaemia, hypotension or renal artery stenosis

Non-steroidal anti-inflammatory drugs (NSAIDs) (eg ibuprofen)

  • Reduce cortical blood flow and glomerular perfusion by blocking production of vasodilating prostaglandins (PGE2 and PGI2) by cyclooxygenase
  • Especially amongst elderly patients
  • NSAIDs contraindicated in hypertension and heart failure
101
Q

what are the 2 main ways drugs can be toxic to the kidneys and give examples of drugs in each category

A

Acute tubular necrosis
- Direct injury to renal tubules – disfunction and death to cells
Aminoglycoside antibiotics (eg gentamicin)
Amphotericin B
Calcineurin inhibitors
Chemotherapy
Acyclovir
Poisons (eg ethylene glycol)
Radiocontrast agents
Bacterial sepsis and renal ischaemia increase risk

Acute interstitial nephritis
-	Hypersensitivity reaction manifesting as inflammation in the interstitial spaces surrounding tubules
Clinical features…
-	Low grade fever
-	Skin rash
-	Eosinophilia
-	Urine sample with protein and white blood cell
-	2/3rds drug induced
Causes
-	Antibiotics
-	NSAIDs
-	PPIs
102
Q

what are drugs/ poisins that directly affect tubular function

A
  • Lithium
    o Competes with other cations in tubular cells
    o Causes polyuria secondary to imparing urine concentrating fucntion
  • Heavy metals (eg lead, mercury, arsenic, cadmium)
    o Impair proximal tubule function
103
Q

compare the therapeutic efficacy of loop vs thiazide diuretics

A
  • loop diuretics eg Furosemide has a higher Emax = higher therapeutic efficacy
  • thiazide diuretics eg Hydrochlorothiazide produces diuresis at lower doses = more potent
104
Q

define renal clearance

A
  • theoretical concept which aims to quantify…
    rate at which a substance is removed from the bloodstream
    “volume of plasma completely cleared of a substance per unit time”
105
Q

how do you calculate renal clearance

A

what volume of plasma would contain the amount of sodium cleared by the urine per minute

106
Q

define glomerular filtration rate

A

Volume of plasma filtered by glomeruli per unit time
- related to the concept of clearance (but more clinically meaningful)

GFR = renal clearance
Can use the measurement of substance in plasma in urine alongside the urine output to calculate the GFR

107
Q

what are the conditions for a substance to be completely lost from plasma to the urine aka can be used to calculate gfr

A

o must not alter GFR
o freely filtered at glomerulus
o not reabsorbed/ actively secreted in nephron
o not metabolised/ produced by kidney

108
Q

what is the equation for measuring GFR

A 
GFR = C(urine) x UO/ c(plasma) 
in units (mL/min)
109
Q

exogenous substances used to calculate GFR

A

Insulin (fructose polymer, MW 5 kDa)
- Continuous IV infusion combined with timed urine collections
- Not generally used outside research
Radioisotope tracers
Iohexol
These are all invasive and time consuming so tend to only resort to them in special cases or when a very accurate GFR is requires

110
Q

endogenous substances used to calculate GFR

A

Cystatin C
Both small, and fully filtered in glomerulus at relatively constant rate
Creatinine
- Some active tubular secretion, long established, cheap
- Creatinine clearance provides an estimate of GFR
- Measure – conc. Creatinine in urine, vol. of urine produced per unit of time (urine output), conc. Of creatinine in plasma
- 24-hour urine collection required
o Collecting urine for this time is inconvenient and errors (mis-timed/ incomplete)
o At vv low GFR less creatinine filtered so creatinine secretion becomes proportionally much larger
o Thus compromises accuracy

111
Q

how can we measure creatinine more accurately when calculating GFR

A

Plasma Creatinine alone
- Has a reciprocal relationship with GFR
- But v. large individual differences eg caused by muscle mass
- Eg – plasma creatinine 80umol/L in 21yr old male with lots of muscle vs thin 80 yr old lady could have same GFR but could mean diff. levels of health
So we use the Cockcroft-Gault Equation
- Plasma creatinine
- Requires weight (plus age, sex)
- Often used to adjust dosing for renally-excreted drugs

112
Q

estimated GFR (eGFR)

A
  • Plasma creatinine measurement only!!!
  • Age and sex
  • Derived from large study of people with renal disease – MDRD study
  • More recent study EPI (CKD epidemiology collaboration)
    o Generates more reliable eGFR
    o Renal disease spotted at an earlier stage
    o Not widely accepted but probably will be in future
113
Q

when is eGFR not applicable

A
  • Children, pregnancy, ?very elderly (as neither study included these groups)
  • Muscle mass extreme (frail, amputee, muscle built)
  • Rapidly changing renal function
  • Very low GFR – eg end-stage renal failure
114
Q

define acute kidney injury

A

Definition – an abrupt loss of renal function, commonly characterised by acute…
- Oliguria and increases in plasma urea and creatinine
Often accompanied by a loss in ability to regulate water, electrolyte and acid-base balance

115
Q

what is the clinical criteria for detection of AKI

A
  • eGFR is not accurate for rapidly changing renal function, although it can be used to pick up rapidly progressive renal failure
  • however for AKI, rely on creatinine and UO
  • creatinine levels vary from person to person so change in creatinine in AKI also varys
    NICE guideline
  • inc. plasma creatinine of;
    o >26 umol/L within 48 hrs needs establishment of creatinine baseline
    o >50% in the last 7 days from previous results (often not done before)
  • UO <0.5 mL/kg/hr for >6 hr in adults
  • (>8hr in children)
116
Q

how can we exclude renal loss of K+ when evaluating electrolyte homeostasis - why is this sometimes not accurate and how can this be overcome

A
  • Spot urine K+ <20mmol/L usually excludes renal loss

BUT often simple “spot” urine does not suffice…
As urine conc. Varies considerably throughout the day
- 2 ways to overcome this…
- 24-hour urine collection
- Measure creatinine (or osmolarity) to correct for variability in urine conc.

117
Q

how can we diagnose suspected diabetes insipidus

A
  • Involves with-holding fluids over several hours
  • Potentially dangerous, must be monitored vv closely (true DI -> hypernatraemia)
  • DI involves failure of action of vasopressin (or ADH)
  • May be cranial or nephrogenic
  • Normal response.- plasma osmolality static, urine osmolality rises ie kidney conc. Urine
  • DI – plasma osmolality rise – urine remains dilute
  • Cranial DI should be responsive to DDAVP (synthetic vasopressin)
118
Q

what can we test for with dipstick urinalysis

A
  • Glucose (diabetes)
  • Ketones (ketoacidosis)
  • Protein (albumin) – not as sensitive as lab measurement
  • Blood (detects Hb)
  • Leukocytes (UTI)
  • Nitrites (produced by nitrate-reducing UTI bacteria)
  • Bilirubin (jaundice)
  • Urobilinogen (absent in cholestatic jaundice)
119
Q

what is microalbuminuria - why is it improtant to detect it, what are normal levels, how does it occur

A
  • Abnormal level of albumin, usually too low for detection by urine dipstick
  • ACR > 3.5 mg/mmol in men, >2.5mg/mmol in women
  • Important for prevention of significant diabetic nephropathy
  • Can occur transiently eg post-trauma, surgery, pyrexia, vigorous physical exercise

YEAR 2 SEMESTER 2 (14 decks)

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