urology Flashcards

1
Q

nervous supply of the ureters

A

autonomic nervous system

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2
Q

lymphatic drainage of ureters

A

left: left para aortic lymph nodes
right: right paracaval and interaortocaval lymph nodes

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3
Q

blood supply of ureter

A

upper part: gonadal and renal
middle part: common iliac and branches of abdominal aorta
distal part: superior vesicle

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4
Q

in which 3 locations is the ureter narrowed

A

pelvic ureteric junction
pelvic brim
where it enters the bladder wall

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5
Q

3 layers of ureter

A

outer: fibrous
middle: muscle
inner: epithelium

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6
Q

which class of organ is the bladder

A

when empty = pelvic organ
when distended = abdomen-pelvic organ (as rises when it fills)

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7
Q

3 layers of bladder

A

outer: loose connective tissue
middle: smooth muscle and elastic fibres
inner: transitional epithelium

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8
Q

blood supply and venous drainage of bladder in females

A

superior and inferior vesical branches of the internal iliac artery
drained by vesical plexus which drains into internal iliac vein

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9
Q

lymphatic drainage of bladder

A

internal iliac nodes then paraaortic nodes

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10
Q

bladder nervous supply

A

autonomic nervous system

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11
Q

describe the internal and external urethral sphincters

A

internal
- at neck of bladder
- thickened detrusor muscle
- smooth muscle
- involuntary control

external
- at external urethral orifice
- skeletal muscle
- voluntary control

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12
Q

blood supply of urethra in females

A

internal pudendal arteries and inferior vesicle branches of the vaginal arteries

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13
Q

lymphatic drainage of urethra in females

A

proximal urethra: internal iliac nodes
distal urethra: superficial inguinal nodes

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14
Q

nervous supply of urethra in females

A

vesical plexus and pudendal nerve

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15
Q

blood supply and venous drainage of bladder in males

A

supplied by superior and inferior vesical branches of internal iliac artery
drained by prostatic venous plexus which drains into internal iliac vein

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16
Q

3 lobes of prostate

A

left lateral
middle
right lateral

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17
Q

prostate blood supply and venous drainage

A

supplied by inferior vesical artery
drained via prostatic plexus to the vesical plexus and internal iliac vein

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18
Q

lymph drainage of prostate

A

internal and sacral nodes

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19
Q

prostate nervous supply

A

autonomic nervous system

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20
Q

3 parts of male urethra

A

prostatic
membranous
spongy

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21
Q

blood supply of male urethra

A

prostatic - inferior vesical artery
membranous - bulbourethral artery
spongy - internal pudendal

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22
Q

lymph drainage of male urethra

A

prostatic and membranous - obturator and internal iliac nodes
spongy - superficial and deep inguinal nodes

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23
Q

nervous supply of male urethra

A

prostatic plexus

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24
Q

what stimulates/inhibits ADH production/secretion

A

stimulated by
- increased plasma osmolarity
- hypovolaemia
- hypotension
- nausea
- Angiotensin II
- nicotine

inhibited by
- decreased plasma osmolarity
- hypervolaemia
- hypertension
- ANP
- ethanol

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25
Q

which urea transporters does ADH/vasopressin increase the numbers of

A

UT-A1
UT-A3

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26
Q

which water channels does ADH regulate the numbers of

A

aquaporin 2 and aquaporin 3

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27
Q

where is ADH produced and stored

A

produced in hypothalamus (neurons in supraoptic and paraventricular nuclei)
stored in posterior pituitary

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28
Q

treatment for central diabetes insipidus

A

external ADH

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29
Q

treatment for SIADH

A

non peptide inhibitors of ADH receptor (eg conivaptan, tolvaptan)

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30
Q

treatment for nephrogenic diabetes insipidus

A

thiazide diuretics and NSAIDs

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31
Q

symptoms for SIADH

A

hyperosmolar urine
hypervolaemia
hyponatraemia

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32
Q

what is the problem in nephrogenic diabetes insipidus

A

less/mutant AQP2 receptors
mutant V2 receptors

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33
Q

which cell in the DCT and CD becomes very important during alkalosis and why

A

beta intercalated cell
mediates H+ reabsorption and HCo3- secretion

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34
Q

mechanism of action of ADH

A

binds to V2 receptor
stimulates G protein signalling cascade
G protein activates adenylate cyclase which catalyses conversion of ATP into cAMP
cAMP leads to protein kinase A production which causes AQP2 production
AQP2 inserts into the apical side of the cell

ADH can also increases AQP3 numbers which insert onto basolateral side of cell

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35
Q

does urea concentration have an effect on ADH production

A

no

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36
Q

which part of nephron is potassium secreted

A

distal nephron

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37
Q

which compartment has the most fluid in the body

A

intracellular

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38
Q

contrast positive and negative water balance

A

positive water balance: have too much water - produce hypoosmotic urine

negative water balance: have too little water - produce hyperosmotic urine

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39
Q

describe countercurrent multiplication

A

water entering loop of Henle is iso-osmotic to medullary interstitium
salt is actively reabsorbed in ascending limb, increasing the osmolarity of the medullary interstitium
this causes water to be passively reabsorbed in the descending limb
new water comes in and pushes this water along, process is continual
end up with an osmotic gradient in the medullary interstitium: most osmotic at bottom of loop of Henle so most water is reabsorbed there

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40
Q

describe urea recycling

A

ADH increases number of UT-A1 and UT-A3

urea leaves collecting duct via UT-A1(apical) and UT-A3 (basolateral)
the urea is now in the medullary interstitium and can either
1) re enter nephron via UT-A2
2) enter blood via UT-B1

this maintains a concentration of urea in the medullary interstitium, which allows water to be reabsorbed

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41
Q

how does ADH support Na+ reabsorption

A

increases Na+ 2Cl- K+ symporter in thick ascending limb
increases Na+ Cl- symporter in DCT
increases Na+ channels in collecting duct

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42
Q

what is antidiuresis and when does it happen

A

concentrated urine in low volume excretion
when there is high ADH

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43
Q

treatment for SIADH

A

non peptide inhibitor of ADH
- conivaptan
- tolvaptan

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44
Q

normal ECF concentration of bicarbonate

A

24 mEq/L

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45
Q

what is the role of kidneys in acid base balance

A

excretion and secretion of H+
reabsorption of bicarbonate
production of new bicarbonate

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46
Q

how much of the bicarbonate freely filtered into the kidneys is reabsorbed

A

almsot 100%

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47
Q

where is most of the bicarbonate reabsorbed in the kidneys

A

proximal convoluted tubule

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48
Q

what is henderson hasselbalchs equation

A

[H+] = (24 x PCo2) / [HCo3-]

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49
Q

contrast the functions of the alpha and beta cells of the DCT and collecting duct

A

alpha = bicarbonate reabsorption, H+ excretion
beta = H+ reabsorption, bicarbonate excretion
(beta cells becomes. esp important during alkalosis)

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50
Q

what is the compensatory mechanism for respiratory alkalosis, respiratory acidosis, metabolic alkalosis, metabolic acidosis

A

met alkalosis: decrease ventilation, increase bicarbonate excretion
met acidosis: increase ventilation, increase bicarbonate production and reabsorption
resp alkalosis: intracellular buffering (acute), decrease bicarbonate reabsorption and production (chronic)
resp acidosis: intracellular buffering (acute), increase bicarbonate reabsorption and production (chronic)

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51
Q

what is an osmole

A

1 osmole = 1 mole of dissolved particles per litre

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52
Q

what is the concentration of ECF

A

290 mosm/L (milli osmoles per litre)

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53
Q

what is the normal osmolarity of plasma

A

285-295 mosm/L

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54
Q

describe central and peripheral regulation of sodium intake

A

central:
via lateral parabrachial nucleus
- in conditions of Na+ deprivation: increases appetite for Na+ via GABA and opioids
- in conditions of euvolemia: decreases Na+ intake via serotonin and glutamate

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55
Q

where is most water and Na+ reabsorbed

A

PCT

56
Q

how to calculate GFR from RPF (renal plasma flow)

A

GFR = 0.2 x RPF (because approximately 20% of renal plasma enters tubular system)

57
Q

what is the best way to retain sodium

A

filter less

58
Q

what is aldosterone released in response to

A

angiotensin II
or
low bp

59
Q

what are the effects of aldosterone

A

increases sodium reabsorption
increases potassium and H+ excretion

60
Q

what is the effect of excess aldosterone

A

hypokalaemic alkalosis

61
Q

what is the filling and voiding stage of urination

A

filling: urethral sphincter sphincter closed, detrusor muscle fills and distends without a rise in intravesical pressure
voiding: muscle contracts, upper urethral sphincter relaxes, urethra opens

62
Q

describe the process of micturition

A

bladder fills and stretches
M3 receptors on detrusor muscle are stretched
S2- 4 parasympathetic fibres release ACh which acts on the M3 receptors, activating them and causing detrusor muscle to contract
the fibres also inhibit internal urethral sphincter, relaxing it and causing it to open

after bladder is emptied, M3 receptors are no longer stretched so are deactivated
T11- L2 sympathetic fibres release noradrenaline which acts on Beta 3 receptors, causing detrusor muscle to relax

63
Q

risk factors for stress incontinence

A

age
obesity
smoking
pregnancy
rout of delivery

64
Q

investigations for stress incontinence

A

stress test
urodynamics - check for urination during an increase in intra abdominal pressure (eg cough) WITHOUT detrusor muscle contractions

65
Q

treatments for stress incontinence

A

FIRST: physio with pelvic floor examinations
if the issue is increased urethral mobility: colposuspension or mid urethral sling
if the issue is impaired urethral closing: periurethral bulking agents

66
Q

causes of stress incontinence

A

impaired urethral closure
impaired urethral and bladder support

67
Q

what is overactive bladder and what are the causes

A

involuntary contractions of detrusor muscle causes urinary urgency and frequency and nocturia, can be with or without urinary urge incontinence

causes: idiopathic, neurogenic, outlet obstruction (irritates the muscle so causes inappropriate contractions)

68
Q

what do you need to exclude if you think the diagnosis may be overactive bladder

A

infection via dip stick and MC&S
prolapse for women
enlarged prostate for men

69
Q

treatment for overactive bladder

A

lifestyle changes
bladder retraining
antimuscarinics
beta 3 agonists
botox
neuromodulation (S3)
surgical: augmentation cystoplasty and urinary diversion

70
Q

what is overflow incontinence and what are the causes

A

chronic retention leading to over flow

  • outlet obstruction (BPH or faecal impaction)
  • neck of bladder stricture
  • urethral stricture
  • under-active detrusor muscle –> atonic bladder
  • DHx (dihydrexine) alpha adrengerics, anticholinergics, sedatives
  • dennervation following surgery
71
Q

what is continuous incontinence and what are the causes

A

continuous involuntary urination
due to vesicovaginal fistula or ectopic urethra (into vagina or ureter)

72
Q

what is BPH and how does it cause lower urinary tract symptoms

A

benign overgrowth of lateral and medial lobes of prostate due to effects of testosterone, compressing urethra and obstructing outflow

73
Q

what are the lower urinary tract symptoms caused by BPH

A

hesitancy
poor flow
dribbling post micturition
frequency and nocturia
acute retention

74
Q

what do you need to exclude before diagnosing BPH

A

cauda equina
bladder or prostate cancer
high pressure chronic retention

75
Q

BPH investigations

A

urodynamics
post void reisdual volume
void diary
bloods: check PSA levels –> indicative of prostate size
USS
cystoscopy to check for cancer

76
Q

BPH investigations

A

urodynamics
post void reisdual volume
void diary
urine dipstick
bloods: check PSA levels –> indicative of prostate size
USS
cystoscopy to check for cancer

77
Q

BPH treatments

A

1) lifestyle changes:
lose weight, avoid constipation. reduce caffeine and fluid intake in evening
2) medication:
- alpha blockers –> alpha 1 adrenergic receptors are found on prostate stromal smooth muscle and neck of bladder. Blocking these can cause relaxation of the muscles
- 5 alpha reductase inhibitors: block the conversion of testosterone to DHT. This prevents prostate growth
3) TURP: transurethral resection of prostate

78
Q

complications of untreated BPH

A

chronic painless retention and overflow incontinence
chronic renal failure (urine goes back up ureters and damages kidneys)

79
Q

how is micturition different in adults vs infants

A

infants: it is a local spinal reflex
adults: higher control centre can keep external urethral sphincter closed until it is appropriate to urinate –> pudendal nerve causes contraction of the sphincter

80
Q

overactive bladder risk factors

A

age
prolapse
IBS
bladder irritants eg caffeine, nicotine
increased BMI

81
Q

what kind of cancer is the most common kidney cancer

A

renal cell carcinoma: adenocarcinoma

82
Q

features of kidney cancer

A

painless visible haemturia / persistent microscopic haematuria
palpable mass
loin pain
metastatic disease symptoms eg bone pain, haemoptysis

83
Q

what do renal function blood tests show for haemturia

A

anaemia (low rbc)
high calcium
high liver enzymes

84
Q

investigations for painless visible haematuria

A

flexible cystoscopy
CT urogram
renal function test

85
Q

investigations for painless visible haematuria

A

flexible cystoscopy
CT urogram
renal function test

86
Q

investigation for invisible haemturia

A

flexible cystoscopy
US of KUB (kidney, ureter, bladder)

87
Q

investigations specifically for suspected kidney cancer

A

CT renal triple phase
staging CT chest
bone scan if symptomatic

88
Q

kidney cancer management

A

partial or radical nephrectomy
if tumour is small and can’t do surgery on the pt: cryosurgery (freeze it, put needle in and oblate it)
metastatic disease: receptor tyrosine kinase inhibitors

89
Q

what kind of cancer is the most common bladder cancer

A

transitional cell carcinoma

90
Q

features of bladder cancer

A

painless visible haematuria
persistent invisible haematuria
suprapubic pain
lower urinary tract symptoms and UTI
metastatic disease features: bone pain, lower limb swelling

91
Q

investigations for bladder cancer

A

if visible haematuria: flexible cystoscopy, CT urogram, renal function test
if non visible: flexible cystoscopy, US KUB

also do biopsy: cystoscopy + transurethral resection of bladder lesion (but this is also treatment as you remove the cancerous tissue then send it for biopsy)

92
Q

bladder cancer management

A

cystoscopy + transurethral resection of bladder lesion (to remove cancer and also test it as you send the tissue off as a biopsy)

if non muscle invading
- cystoscopic surveillance
- chemotherapy
- BCG (immunotherapy)

if muscle invading
- radiotherapy
- chemo therapy
- cystectomy
- palliative treatment

93
Q

what kind of cancer is the most common prostate cancer

A

adenocarcinoma

94
Q

features of prostate cancer

A

asymptomatic unless metastasises

95
Q

investigations for prostate cancer

A

bloods: check for high PSA (although this isn’t specific for prostate cancer - can be high in other things too eg infection, BPH)
MRI and THEN a biopsy
transperineal prostate biopsy

96
Q

bladder cancer management for a high grade and low grade cancer in a young and fit pt vs an old and unfit

A

young and fit:
- high grade: radical prostatectomy / Radiotherapy
- low grade: active surveillance - biopsy, PSA, MRI

old and unfit
- high grade: hormone therapy
- low grade: watchful waiting - regular PSA testing

97
Q

prostate cancer treatment side effects

A

surgical prostatectomy carries a risk of damaging proximal urethral sphincter and also cavernous nerves
- risk of incontinence and erectile dysfunction

98
Q

risk factors for prostate cancer

A

increasing age
westen - scandenavian - countries
African american ethnicity

99
Q

why is transperineal prostate biopsy used instead of transrectal

A

less risk of infection
more able to sample all areas of the prostate

100
Q

what are the 6 types of germ cell tumours in testicular cancer

A

seminoma
spermatocytic seminoma
teratoma differentiated
embryonal carcinoma group
yolk sac tumour
choriocarcinoma

(the first two are seminomatous germ cell tumours, the last 4 are non seminomatous germ cell tumorus)

101
Q

what are the 5 types of sex cord/ gonadal stromal tumours in testicular cancer

A

leydig cell tumour
granulosa cell tumour
Sertoli cell tumour
tumours of fibroma / thecoma
mixed tumours

102
Q

what are stages 1A, 1B and 1S in testicular cancer

A

1A: no signs of local invasion or metastases. serum tumour markers are normal after orchiectomy (testes removal)
1B: signs of local invasion but not of metastases
1S: signs of local invasion and of metastases - serum tumour markers are still abnormally high after orchiectomy

103
Q

what are the 3 principal serum tumour markers in testicular cancer

A

AFP: alpha fetoprotein
HCG: beta subunit of human chorionic gonadotrophin
LDH: lactate dehydrogenase

104
Q

what kind of cancers is alpha fetoprotein tumour marker found in

A

teratomatous germ cell tumour with a yolk sac component

105
Q

what kind of cancers is HCG tumour marker found in

A

germ cell tumours containing syncitiotrophoblast cells
all choriocarcinomas
some seminomas

106
Q

what kind of cancers is LDH tumour marker found in

A

not specific to any type

107
Q

how to approach the diagnosis of testicular cancer

A

ultrasound
biopsy
surgery and chemo
assess serum tumour markers to stage the cancer
check surrounding structures/ lymph nodes
instruct pt how to do regular self examination

108
Q

what is the difference in how you should treat seminoma germ cell tumours vs non seminoma germ cell tumours

A

seminoma germ cell tumours respond well to radiotherapy, non seminoma tumours do not

109
Q

name some penile disorders which can make it hard for erection

A

tight frenulum - hard for tip to come out
phimosis - tight skin which is difficult retract
para-phimosis - skin retracts but is stuck in retracted position

110
Q

how to fix para phimosis

A

manual pressure
dextrose soaked gauze
dundee technique
dorsal slit

111
Q

what is genital lichen sclerosis and how does it present

A

chronic inflammatory dermatosis

  • phimosis
  • meatal stenosis - spraying of stream
  • urethral stricture
  • from white plaques with epidermal atrophy and scarring
  • red cracked blistered bleeding skin
112
Q

management of genital lichen sclerosis

A

non soap wash eg dermal
emollients
barrier cream
very strong topical steroids eg dermovate
weight loss

113
Q

treatment for erectile dysfunction as a result of radical prostatectomy

A

PDE5 inhibitors
prostaglandin E1 injections
penile prosthesis devices

114
Q

treatment for incontinence as a result of radical prostatectomy

A

build pelvic floor muscles
artificial urethral sphincter implants

115
Q

what should the PSA level be after prostatectomy

A

<0.01 ng/ml (higher = relapse)

116
Q

two models used to convert creatinine into GFR

A

MDRD - modification of diet in renal disease
CKD-EPI - CKD epidemiology collaboration

117
Q

what is the Kidney failure risk equation

A

an equation used to predict the chance of needing a kidney transplant in 2-5 years in someone with stable CKD
takes into account age, sex, eGFR, ACR
used to improve pt understanding of their disease and to identify high risk pts

118
Q

what are two precautions CKD pts should take when it comes to blood giving and receiving

A

shouldn’t receive any blood transfusions as could make a future transplantation be rejected
if having blood taken, don’t let them put it into antecubital fossa as this is needed for dialysis of they need that in the future, use veins on back of hand instead

119
Q

is urea a good method of assessing GFR and why

A

no
confounded by diet, catabolic state, liver enzymes, drugs, GI bleeding

120
Q

is creatinine a good method of assessing GFR and why

A

trend is useful in context of that particular patient
as it is confounded by age, sex, muscle mass, race

121
Q

is creatinine clearance good method of assessing GFR and why

A

no
difficult for older people to take measurements
over estimates GFR at low GFRs

122
Q

are radionuclide studies a good method of assessing GFR and why

A

yes
reliable but expensive

123
Q

is inulin clearance a good method of assessing GFR and why

A

difficult/long to do
so used only in research

124
Q

initial management for kidney failure

A

fix fluid balance
- hypovolaemia = give fluids
- hypervolameia = diuretics

fix hyperkalaemia
- drive into cells = sodium bicarbonate, insulin dextrose
- excrete = diuretics
- increase GI absorption = potassium binders

125
Q

conservative management for kidney failure

A

(after fixing fluid and potassium balance)
EPO injections
phosphate binders
vit D supplements

126
Q

how does kidney failure cause hyperparathyroidism

A

CKD
–> 1,25 vit D deficiency and phosphate retention
–> hypocalcaemia
–> hyperparathyroidism

127
Q

how does kidney failure cause anaemia

A

reduced EPO production

128
Q

what is the arterial blood gas in kidney failure

A

metabolic acidosis with respiratory compensation

129
Q

how does kidney failure cause hyperkalaemia

A

1) acidosis: H+ ions move into cell and drive K+ out of cell
- get muscle catabolism and anorexia
2) reduced excretion of K+ in kidneys
- cardiac arrhythmias
- muscular and neural effects
- vomiting

130
Q

hyperkalaemia on ECG

A

peaked t waves
broadened or disappearing p waves
wide QRS
asystole
heart block

131
Q

what is Kussmauls respiration

A

in kidney failure, H+ is high
so it is converted H+ + HCO3- –> H2Co3 –> H20 + CO2
high CO2 causes increased resp rate

132
Q

what causes increased CVD risk in kidney failure

A

reduced EPO - anaemia
reduce 1,25 vit D - hypocalcaemia, hyperparathyroidism

133
Q

contrast haemodialysis and peritoneal dialysis

A

haemodialysis:
blood then out of your body and filtered outside via a dialyse filled with dialysate
need to go to a centre for it - 3/4 hrs 3 days a week
strict dietary restrictions
need an access point: either a arteriovenous fistula does under anaesthetic or a central venous line –> risk of bacteraemia

peritoneal dialysis:
blood is filtered inside your body - dialysate is drained in and then out
can do at home, work, travelling
2/3 hrs 7 days a week
less dietary restrictions
risk of infection

134
Q

what 3 things are done to check if a kidney is able to be donated

A

blood type compatibility
HLA (human leukocyte antigen) typing
serum cross matching

135
Q

what should pt avoid after a kidney transplant

A

alcohol
smoking
recreational drugs
live vaccines
NSAIDs
raw meat/fish etc
seville oranges, grapefruit, earl grey tea –> interact with immunosuppressants

136
Q

why do most diuretics increase potassium excretion

A

they increase flow rate
this is detected int he collecting duct and stimulates K+ excretion