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BRS 2 > renal > Flashcards

renal Flashcards

1
Q

osmolarity =

A

concentration x no. dissociated particles

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2
Q

body fluid distribution?

A

2/3 ICF

1/3 ECF - 1/4 intravascular plasma, 3/4 extravascular - 95% interstitial fluid, 5% transcellular

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3
Q

two types of water loss?

A

unregulated - swear, faeces, vomit, water evaporation

regulated - renal urine production

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4
Q

outline positive water balance?

A

high water intake → ↑ ECF , ↓ Na conc, ↓ osmolarity → hypoosmotic urine production → osmolarity normalises

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5
Q

where is most water reabsorbed in the nephron?

A

PCT - 67%

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6
Q

loop of henle, what’s reabsorbed where?

A

descending limb - water passively reabsorbed 15%
thin ascending limb - nacl passively reabsorbed
thick ascending limb - nacl actively reabsorbed

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7
Q

outline the mechanism that optimises water reabsorption in the nephron?

A

countercurrent multiplication
active salt reabsorption in ascending limb→ hyperosmolar medullary interstitium → passive water reabsorption in descending limb

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8
Q

outline urea recycling

A

urea is freely filtered into the nephron via the glomerulus
in pct it is reabsorbed but in the thin descending limb it is the secreted back via the UT-A2 transporter so its concentration increases in. ascending limb and early dct impermeable to urea so concentration stays the same. in late dct urea is rebaoarbed into interstitum via UT-A3 and UT-A1 transporters to increase interstitial osmolarity and so water passively follows

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9
Q

what hormone up regulates UT-A1&3 transporters? and where?

A

ADH on the collecting duct

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10
Q

where is adh produced?

A

supraoptic and paraventricular hypothalamic nuclei

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11
Q

what are the factors affecting adh production?

A 
stimulatory:
hypovolaemia
hyperosmolarity
hypotension
nausea angiotensin II
nicotine
inhibitory:
hypoosmolarity
hypervolemia
hypertension 
ethanol
atrial natriuretic peptide
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12
Q

what is the normal range for plasma osmolarity?

A

275-290 mOsm/kg h2o

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13
Q

mechanism of action of ADH?

A

bins to v2 receptor on basolateral membrane of principal cell → activates g protein which activates adenylate cyclase to produce cAMP → protein kinase A → ↑ secretion of aquaporin 2 channels → transported to apical membrane so more water can be reabsorbed

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14
Q

which water transporters are found on the basolateral membrane of principal cells?

A

AQP3 and AQP4

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15
Q

what is diuresis?

A

increased excretion of dilute urine

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16
Q

how is NaCl reabsorbed in the thick ascending limb?

A

nakstpase pump actively transports na+ into blood → low concentration in cell → na+ moves from tubular fluid into cell with k+ and cl- via na+k+cl- symporter → k+ and cl- move put via k+cl- symporter

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17
Q

how is na+ reabsorbed in collecting duct principal duct?

A

via na+k+atpase pump

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18
Q

role of adh in antidiuresis?

A

supports na+ reabsorption
↑ na+k+cl- symporter in pct
↑ na+cl- symporter in dct
↑ na+ channel in cd

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19
Q

cause features and treatment of cranial DI?

A

decreased/no production and release of adh
polyuria and polydypsia
give external ADH

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20
Q

cause features and treatment of naphrogenic DI?

A

mutant AQP2 or v2 receptor
polyuria and polydipsia
give thiazide diuretics and NSAIDs

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21
Q

cause features and treatment of syndrome of inappropriate ADH secretion (SIADH)?

A 
↑ production  and release of ADH
hyperosomolar urine
hypervolaemia
hyponatraemia 
give a vaptan (non-peptide inhibitor of ADH receptor)
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22
Q

role of kidneys in acid base homestasis?

A

secretion and excretion of H+
reabsorption of HCO3-
production of new HCO3-

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23
Q

where are most HCO3- ions reabsorbed?

A

PCT of nephron

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24
Q

outline the reabsorption of bicarbonate ions in the pct?

A

co2 enters cell via diffusion , combines with water in presence of carbonic anhydrase → HCO3- and H
H+ transported into tubualr fluid via Na+H+ anti porter or H+ATPase pump → H+ recombines with HCO3- to form h20 and co2 → co2 renters cell and process goes on
hco3- leaves cell via na+hco3- symporter to enter blood

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25
Q

difference between a and B intercalated cells?

A

found in dct and cd
a = hco3- reabsorption and h+ secretion
B = hco3- secretion and h+ reabsorption

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26
Q

what transporters are used to move hco3- out of intercalated cells?

A

cl-hco3- antiporter

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27
Q

how are new bicarbonate ions produced in the pct?

A

from glutamine breakdown which gives 2 NH4+ ions and 2 hCO3- ions
hco3- → blood
nh4+ → tubular fluid via na+NH4+ antiporter OR broken down into NH3 and H+ and moved into tubular fluid

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28
Q

how are new bicarbonate ions produced in the dct and cd?

A

the H+ ions secreted from a-intercalated cells combine with HPO42- ions in the tubular fluid instead of recombining with hco3- so there is a net gain of one hco3- ion

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29
Q

what are the homeostatic consequences of kidney failure?

A 
hyperkalaemia
hyponatraemia
low bicarb
metabolic acidosis
hyperphosphataemia → pruritus 
salt and water imbalance
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30
Q

what are the endocrine consequences of kidney failure?

A

↓ 1-a-hydreoxcy;ase → low vitamin D → ↓ Ca2+ → high PTH

low erythropoietin → anaemia

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31
Q

what are the excretory consequences of kidney failure?

A

high urea and creatinine

reduced insulin requirement for diabetic as less is secreted

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32
Q

how would the breathing of someone with kidney failure be? why?

A 
tachypnoeic - kussmaul breathing
respiratory compensation for metabolic acidosis 
normal o2 sats
low pCO2
high pO2
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33
Q

classic presentations of someone with renal failure?

A 
hypovolaemia - poor skin turgor and ↓ cap refill
tachypneic
acidosis
hyponatraemia
↑ urea and creatinine
anaemia - pale 
lethargy
anorexia
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34
Q

what can kidney failure lead to?

A

hypertension
oedema
pulmonary oedema

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35
Q

symptoms of hyperkalaemia?

A

arrythmias
vomitting
neural/muscular activity

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36
Q

what ecg changes would you see with hyperkalaemia?

A 
peaked t waves
wide/shorter/disappeared p waves
wide QRS
heart block
asystole
vt/vf
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37
Q

how can kidney failure lead to hyperparathyroidism?

A

kidney failure → reduced vit d levels → ↓ intestinal ca2+ absorption → hypocalcaemia → hyperparathyroidism

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38
Q

what are people with CKD most likely to die from?

A

CVD

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39
Q

initial management of kidney failure?

A

fluid management

  • hypovolaemic: give fluids
  • hypervolaemic: trial diuretics/dialysis

hyperkalaemia

  • move k+ into cells : sodium bicarb. / insulin dextrose
  • move k+ out of body : diuretics/dialysis
  • reduce gut absorption : potassium binders
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40
Q

long - term management of kidney failure?

A 
erythropoietin injections - help anaemia
diuretics - for hypertension
phosphate binders - for ↑k+
1,25 vit d supplements
symptom management

haemodialysis
peritoneal dialysis
transplantation

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41
Q

why should transfusions sometimes be avoided in kidney disease patients?

A

if they’re transplantable a transfusion can cause sensitisation (HLA) which can lead to transplant failure

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42
Q

what veins should be avoided in kidney failure patients why?

A

antecubital fossa and cephalic vein
use veins on back of hand instead
in case pt needs a fistula

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43
Q

what are the options for assessing GFR?

A

urea - poor indicator, confounded by diet, liver fx etc
creatinine - affected by muscle, race, sex, helpful if trend
radionuclide studies - reliable but expensive
creatinine clearance - difficult in elderly, overestimates GFR at low GFR§
inulin clearance - laborious, research only

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44
Q

normal GFR range?

A

≥60 ml/min/1.73m2

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45
Q

normal ACR?

A

<3 mg/mmol

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46
Q

normal plasma osmolality?

A

285 - 295 mosmol/L

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47
Q

most prevalent ion in ECF and conc?

A

sodium 140mmol/L

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48
Q

what part of the brain regulates sodium intake?

A

lateral parabrachial nucleus

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49
Q

sodium absorption in the nephron and %?

A 
pct - 67
TAL - 25
dct - 5
cd - 3 
excretion <1
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50
Q

what percentage of renal plasma enters the tubular system?

A

20↓

→ GFR = RPF * 0.2

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51
Q

what happens when theres high tubular sodium?

A

increased sodium chloride uptake by triple transporter (K+na+cl-) → adenosine released from macula dense cells → detected by extraglomerular mesangial cells → ↓ renin production → afferent smc contraction → ↓ perfusion pressure → ↓ GFR → ↓ na+ filtered and reabsorbed → ↓ tubular na+
↓ renin → ↓ angiotensin II & aldosterone

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52
Q

what promotes the reabsorption of na+?

A

increased sympathetic activity (from low bp) on PCT, JGA and glomerulus
increased renin → ↑ angiotensin II (PCT) → ↑aldosterone (DCT & CD)
low tubular na+ → JGA → ↑renin

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53
Q

what hormone inhibits renin secretion?

A

atrial natriuretic peptide secreted in response to atrial stretch

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54
Q

what stimulates the release of aldosterone? from where?

A

angiotensin II and ↓ BP via baroreceptors
up regulate aldosterone synthase
zona glomerulosa of adrenal cortex

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55
Q

what does aldosterone stimulate?

A

sodium reabsorption
potassium excretion
h+ excretion

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56
Q

what can aldosterone excess lead to?

A

hypokalaemic alkalosis

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57
Q

how does aldosterone work?

A

binds to mineralocorticoid receptor and unregulated the expression of sodium channels at apical membrane and na+k+atpase at basolateral membrane in collecting duct

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58
Q

outline hypoaldosteronism?

A

reduced reabsorption if na+ in detail tubule → ↑ excretion of na+ and water → ECF volume falls → ↑ renin, ang II and ADH

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59
Q

symptoms of hypoaldosteronism?

A

dizziness
low bp
salt craving
palpitations (hyperkalaemia)

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60
Q

symptoms of hyperaldosteronism?

A

high blood pressure
muscle weakness
polyuria
thirst

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61
Q

outline Liddle’s disease?

A

inherited disease of high bp
mutation in aldosterone activated sodium channels in principal cells so it is always activated → sodium retention → hypertension

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62
Q

low pressure baroreceptors?

A

in the heart, can detect low and high pressures
atria
pulmonary artery
right ventricle

63
Q

high pressure baroreceptors?

A 
vascalature
only low pressure
aortic arch
carotid sinus
JGA
64
Q

what happens with baroreceptors when bp is low?

A

reduced barorecpetor firing → afferent fibre signals to brainstem → ↑ sympathetic activity and ADH release
JGA cells activated → ↑ renin (high pressure side only)

65
Q

what are the actions of ANP?

A

afferent arteriole dilation (and of other vessels) → ↑ GFR
inhibition of sodium reabsorption in pct and cd
inhibits renin and aldosterone release
↓ bp

66
Q

what are the effects of ACE inhibitors?

A

vasodilation → ↑ vascular volume → ↓ BP
↓ na+ reabsorption in pct → more in distal tubule
↓ aldosterone → ↓ na+ uptake in cct → more in distal tubule
== ↓ water reabsorption → ↓ BP

67
Q

name 5 types of diuretics and where they act?

A 
osmotic diuretics - pct , mannitol
carbonic anhydrase inhibitors - pct , acetazolamide
loop diuretics - LoH tal , furosemide
thiazides - dct
k+ sparring diuretics - cd
68
Q

MOA of carbonic anhydrase inhibitors?

A

acts n carbonic anhydrase in pct

relies on fact that some sodium is exchanged for h+ ions which is made from carbonic anhydrase activity on h2xo3

69
Q

why carbonic anhydrase inhibitors not lead to a bigger natriuresis?

A
  1. still sodium being exchanged for bicarbonate ions
  2. increased reabsorption of sodium in tal, dct and cd
  3. macula densa detects increased tubular sodium and reduces gfr (tubuloglomerular feedback)
70
Q

what acid base disturbance can carbonic anhydrase inhibitors lead to?

A

metabolic acidosis (less H+ being screwed into urine in exchange for sodium)

71
Q

moa of loop diuretics?

A

inhibit triple transporter (na+-k+-2cl- symporter) in apical membrane of TAL of LoH → ↓ Na+ uptake → ↑ Na+ in distal nephron → ↓ reduced water uptake (medullary interstitial osmolality decreases)

72
Q

moa of thiazides?

A

block the na-cl symporter on the apical membrane of cells of the distal tubule → less na+ reabsorption in DCT → ↑ na+ in distal tubule → less water reabsorption

73
Q

thiazides can cause increased reabsorption of which ion? how?

A

calcium
as na-k-atpase still works, there is an increased na+ gradient across the basolateral membrane in distal tubule cells
in response sodium ions are transported back into cells via the na+-ca2+ anti porter - this creates a ca2+ gradient at the apical membrane so more ca2+ is reabsorbed and serum calcium levels increase

74
Q

moa of k+ sparing diuretics?

A

aldosterone antagonists - prevent aldosterone form binding to the mineralocorticoid receptors on principal cells in the cortical collecting duct → ↓ ENaC and Na/K/ATPase on the apical membranes → less na+ reuptake and K+ secretion

75
Q

2 examples of a k+ sparing diuretic? what else is it used to treat?

A

spironolactone and eplerenone

conn’s syndrome (hyperaldosteronism)

76
Q

extracellular vs intracellular [k+]?

A

150 vs 3-5 mmol/L

77
Q

which hormones stimulate k+ uptake into tissues?

A

insulin
aldosterone
adrenaline

78
Q

what stimulates k+ secretion in the kidneys?

A

↑ [k+]
↑ aldosterone
↑ tubular flow
↑ plasma pH

79
Q

how does increased flow lead to ↑ k+ secretion?

A

the flow bends cilia on the apical membrane who activates a PDK1 channel so more ca2+ enters the cell → ↑ ca2+ activates k+ channels so more k+ is secreted

80
Q

what can cause hypokalaemia?

A 
inadequate dietary intake
diuretics (increase tubular flow rate)
surreptitious vomitting
diarrhoea
genetics eg.Gitelmans syndrome
81
Q

risk factors for hyperkalaemia?

A 
k+ sparing diuretics
ACE inhibitors
elderly
severe diabtees
kidney disease
82
Q

most common type of kidney cancer?

A

renal cell carcinoma

83
Q

risk macros for kidney cancer?

A 
smoking
overweight
dialysis
hypertension
genetics
84
Q

red flag symptom for urological cancer?

A

painless haemturia / persistent microscopic haematuria

85
Q

symptoms/signs of RCC?

A

hameturia
loin/flank pain
palpable abd mass
metastatic symptoms - bone pain, weight loss, haemoptysis

86
Q

investigations for a pt with visible haematuria?

A

flexible cystoscopy
ct urogram
renal function tests

87
Q

investigations for a pt with non-visible haematuria?

A

flexible cytoscopy

US KUB

88
Q

investigations for a pt w suspected kidney cancer?

A

CT renal triple phase
staging - CT chest
bone scan if symptomatic

89
Q

TNM staging of RCC?

A

T1 ≤7cm
T2 ≥7cm
T3 extra renal but inside adrenal/perinephric fascia
T4 beyond perninephric fascia into surrounds

N1 met in single regional LN
N2 mets in ≥2 regional LN

M1 - distant met

90
Q

what other staging is used for RCC?

A

fuhrman grade
1-4
differentiation well to poorly

91
Q

gold standard management for kidney cancer?

A 
excision via :
partial nephrectomy (if pt has single kidney, bilateral tumours, multifocal RCC, T1 tumours)

radical nephrectomy

92
Q

management for kidney cancer patients unfit for surgery?

A

cryosurgery

93
Q

mangament for patients with metastatic kidney disease/

A

receptor tyrosine kinase inhibitors

94
Q

commonest type of bladder cancer?

A

transitional cell carcinoma

squamous cell carcinoma where schistosomiasis is endemic

95
Q

risk factors for bladder cancer?

A

smoking
radiation
chronic catheterization
schistosomiasis

96
Q

signs/symtpms of bladder cancer?

A

painless haematuria - visible/microscopic
suprapubic pain
lower urinary tract symptoms - polyuria
metastatic disease symptoms - bone pain, lower limb swelling

97
Q

bladder cancer TNM staging?

A 
Ta - non invasive papillary carcinoma
Tis - carcinoma in situ
T1 - sub epithelial connective tissue
T2 - muscular propria
T3 - perivesical aft 
T4 - prostate, uterus, vagina, bowel, abdo

N1 - 1 LN below common iliac bifurcation
N2 - ≥1 LN “”
M1 - distant mets

98
Q

other classification method for bladder cancer?

A

WHO
G1 - G3
well , moderate, poorly differentiated

99
Q

management for non muscle invasive bladder cancers?

A

transurethral resection of bladder lesion (can also be used histologically) ± intravesciular chemotherapy/ BCG immunotherapy

100
Q

management for muscle invasive bladder cancers?

A

cystectomy
radiotherapy
±chemo
palliative

101
Q

commonest typer of prostate cancer?

A

adenocarcinoma

102
Q

risk factors for prostate cancer?

A

age
scandinavian
african americans

103
Q

how does prostate cancer usually present?

A

asymptomatic unless metastatic

104
Q

risk of using PSA to diagnose prostate cancer?

A

prostate specific but not prostate cancer specific

can be raised in UTI, prostatitis, BPH, age

105
Q

investigations for prostate cancer?

A

blood tests for PSA
MRI
transperineal prostate biopsy

106
Q

TNM staging of prostate cancer?

A

T1 non-palpable
T2 palpable
T3 into periprostatic fat
T4 invaded onto adjacent structure

N1 pelvic LN

M1a non regional LN
M1b bone
M1x other sites

107
Q

what other criteria can be used to grade prostate cancer?

A

Gleason score
2-6 = well differentiared
7 - moderate
9 - poor

108
Q

management for prostate cancer?

A

young/fit + high grdae - radcial prostatectomy/radio
young/fit + low grade - active surveillance (PSA, MRI Bx)

old/unfit + high grade - hormone therapy
old/unfit + low grade - regular PSA testing

109
Q

what needs to be monitored post-prostatectomy?

A

PSA - should be undetectable or <0.01ng/ml

≥0.2 = relapse

110
Q

side effects of prostate cancer treatment?

A

prostatatectomy removes proximal urethral sphincter and reduces urethral length - incontinence
risk of damage to cavernous nerves - ED

111
Q

which 3 places are the ureters constricted?

A

pelvic ureteric junction
pelvic brim
ureterovesical juction

112
Q

3 layers of ureteric tissue?

A

outer fibrous tissue
middle muscle layer
inner epithelium layer

113
Q

3 layers of bladder tissue?

A

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

114
Q

length of female vs male urethra?

A

3-4 cm vs 20cm

115
Q

function of the prostate?

A

secretes seminal fluid to liquify coagulated semen

116
Q

lymph nodes of bladder?

A

internal iliac → paraaortic nodes

117
Q

lymph nodes if prostate?

A

internal and sacral nodes

118
Q

3 parts to male urethra?

A

prostatic
membranous
spongy

119
Q

explain normal micturition

A

bladder fills and distends without rise in intravesical pressure
urethral sphincter is contracted and urethra is closed
to void bladder contracts and urethral sphincter relaxes and urethra opens

120
Q

how does micturition vary between infants and adults?

A

infants : local spinal reflex where bladder empties upon reaching critical pressure
adults : voluntary control by higher centre control of external urethral sphincter keeping it closed

121
Q

explain the innervation involved in micturition

A

as bladder fills M3 receptors are stimulated (PSNS S2-4)
they become stretched which leads to contraction of detrusor muscle
parasympathetic fibres also inhibit the internal urethral sphincter which causes it to relax and the urethra to open
=bladder emptying

bladder empties and stretch fibres become inactivated
→ sympathetic (T11-L2) NS is stimulated to activate beta 3 receptors causing relaxation of detrusor muscle so bladder can refill

122
Q

types of urinary incontinence?

A 
stress
urge
overflow
continuous
functional
mixed
123
Q

define stress urinary incontinence?

A

involuntary leakage on effort/exertion/sneezing/coughing

124
Q

risk factors for stress UI?

A 
women
older age
obesity
smoking
pregnancy and route of delivery
125
Q

pathology of stress UI?

A

impaired bladder and urethrap support

impaired urethral closure

126
Q

investigations for stress UI?

A

postive stress test (loss of urine on examination)

urodynamics - leakage during increase in intraabdominal pressure with absence of detrusor contraction

127
Q

management of stress UI?

A

reduce weight
physio with PFE
Sx : mid urethral sling, colposuspension, periurethral bulking agents

128
Q

risk factors for urge UI?

A 
age
prolapse
increased BMI
IBS
bladder irritants - caffeine, nicotine
129
Q

pathology of UI

A

involuntary detrusor contractions

idiopathic/neurogenic/bladder outlet obstruction

130
Q

signs and symptoms of an overactive bladder?

A 
urgency and frequency
nocturia
urgency incontinence
↓ QOL - sleep disorder, anxiety, depression
enlarged prostate/prolapses
131
Q

investigations for an overactive bladder?

A

urine dipstick - infection?
voiding diaries and post void residual
urodynamics
cystoscopy

132
Q

management for overactive bladder?

A 
lifestyle changes 
bladder retraining
antimuscarinic drugs 
beta 3 agonists
botox - paralyses detrusor 
neuromodulation
sx : augmentation cystoscopy and urinary diversion
133
Q

why would antimuscarinic drugs be given in urge incontinence?

A

it is M3 receptors that are stimulated when the ladder fills and distends - this activates the PSNS so the detrusor contacts and the inter sphincter relaxes to empty the bladder
blocking these receptors would inhibit this process to reduce incontinence

134
Q

why would beta 3 agonist drugs be given in urge incontinence?

A

beta 3 receptors part of the sympathetic nervous system are responsible for relaxing the detrusor muscle while the bladder fills and for contracting the internal urethral sphincter keeping the urethra closed - beta 3 agonists would upregulate this process and prevent the bladder emptying

135
Q

what is overflow incontinecnce?

A

involuntary leakage of urine when bladder is full (±due to chronic retention)

136
Q

causes of overflow incontinence?

A 
outlet obstruction eg BPH
underachieve detrsuor
bladder neck/urethral stricture 
drugs - alpha adrenegics, anticholinergics, sedatives
bladder denervation post surgery
137
Q

what can cause continuous incontince?

A

vesicovaginal fistula

ectopic ureter - straight from kidney to urethra/vagina

138
Q

what is bph?

A

benign prostatic hyperplasia (non-malignant)

139
Q

pathology of bph?

A

hyperplasia of lateral and median lobes → compression of urethra → bladder outflow obstruction

140
Q

signs and symptoms of BPH?

A 
hesitancy 
poor stream
dribbling 
frequency
nocturia
±acute retention
141
Q

differentials for BPH symptoms?

A 
bladder/prostate cancer
cauda equina 
high pressure chronic retention
UTIs
prostatitis 
neurogenic bladder
stones
strictures
142
Q

investigations for BPH?

A 
urine dip
post void residual
voiding diary
bloods - PSA (predict prostate volume)
US 
urodynamics and flow studies
cystoscopy (if worry about cancer)
143
Q

lifestyle management of bph?

A

↓ weight, ↓ caffeine and fluid intake in evening, avoid constipation

144
Q

medical management of bph?

A

alpha blocker - block alpha 1-AR on prostate and bladder neck smooth muscle → relaxation → improved urinary flow rate

5- alpha reductase inhibitors - prevent conversion of testosterone to DHT (promotes growth of prostate) → shrinkage → improved flow rate and less obstructive symptoms

145
Q

surgical management of bph?

A

transurethral resection of the prostate - debunks prostate → better flow

146
Q

what are the complications of bph?

A

progressive bladder distention → chronic retention → overflow incontinence
bilateral upper tract obstruction → renal impairment → CKD

147
Q

why is imaging favoured over biopsies in suspected prostate cancer?

A

random biopsies were associated with under detection of high grade cancer and over detection of low grade cancer

148
Q

what is the common active surveillance protocol for prostate cancer?

A

quarterly PSA testing and DREs

annual MRI with prostate biopsies

149
Q

treatment options for ED resulting from prostatectomy?

A

PDE5 inhibitors
prostaglandin E1 injections
penile prosthesis

150
Q

how does liver cirrhosis lead to high urine osmolarity?

A

hepatic cirrhosis → vasodilation → ↓ systemic vascular resistance → ↓ BP → ↑ ADH secretion → more water reabsorbed and less excreted via urine → ↑ urine osmolarity ↓ hyponatraemia

151
Q

what solute has no effect on ADH?

A

urea

152
Q

compare hemodialysis with peritoneal dialysis

A 
haemodyalysis:
usually dialysis centre visits
3-4.5 hrs 3x/week
strictly dietary constraints
salt water restrictions 
arteriovenous fistula or tunneled central venous line (risk of infection)
peritoneal dialysis:
at home
7 days/week
less food/water constraints 
can travel easily 
can be done anywhere 
risk of peritonitis
153
Q

what factors are considered for being a live kidney donor?

A

fHx of kidney disease
age
comorbidities
kidney match - blood type, HLA typing, serum crossmatch
future pregnancy?
mental health
2 healthy kidneys - size, eGFR, no haem/proteinuria

154
Q

recommendations for post transplant success?

A

minimise risk 9f diabetes, CVD, cancer and psychiatric disorders
low sugar and salt diet
no smoking, NSAIDs, live vaccines, drugs
avoid seville oranges - interact w immunosuppressants
no raw meat, eggs, fish

BRS 2 (12 decks)

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