Urology and renal Flashcards
what are the mechanisms to regulate sodium intake (2)
central
peripheral
how central mechanism regulate sodium intake
- increase appeptite for na+
- lateral parabrachial nucleus suppress desire for Na+ intake
- euvolemia
- inhibition of Na+ intake by serotonin glutamate
how peripheral mechanism regulate sodium intake
taste
where is sodium reabsorbed in nephron
PCT
thick ascending limb
DCT
collecting duct
what happens when there is increased tubular sodium and GFR
- higher tubular sodium
- increased Na/Cl uptake via triple transporter
- Adenosine release from Macula Densa cells
- Detected by extraglomerular mesangial cells
- reduces renin production
- promote afferent SMC contraction
- reduces perfusion pressure and GFR
role of juxtaglomerular cells
secrete renin
how increased SNS activity control sodium excretion
increased reabsorption at collecting duct, PCT, LOH, DCT
reduce GFR rate
stimulate JGA produce more renin
how Angiotensin ll control sodium excretion
increased reabsorption at PCT
increase aldosterone from adrenal gland to increase reabsorption at collecting duct
what is the main vasodilator to control sodium excretion
atrial naturietic peptide (ANP)
ANP role on decrease Na reabsorption
inhibit PCT, LOH, JGA, DCT, CT
when low sodium, will there be more angiotensin l or less
more
when low sodium, will there be more vasoconstriction or less
more
where is aldosterone made and released
adrenal cortex zona glomerulosa
what is aldosterone release in response to
angiotensin ll when decrease in BP via baroreceptors
function of aldosterone for ions (3)
increase Na reabsorption
increase K+ secretion
increase H+ secretion
what happens when aldosterone excess
hypokalaemic alkalosis
why steroid can pass through membrane
steroid hormone
lipid soluble
how aldosterone work in cells
aldosterone bind to mineralcorticoid receptor
translocate into nucleus
then bind to DNA for transcription
what happens when aldosterone increase in cortical collecting duct
increase active na+ channel
what happens in hypoaldosteronism
reduced Na reabsorption in distal nephron
increase urinary Na+ loss
ECF volume falls
increased renin and angiotensin ll and ADH
symptoms of hypoaldosteronism
dizzy
low BP
salt craving
palpitations
what happens in hyperaldosteronism
increased reabsorption of Na in distal nephron
reduced Na urinary loss
ECF volume increases
reduced renin, angiontensin ll and ADH
increase ANP, BNP
what increases in hyperaldosterone
BP
ANP
BNP
symptoms of hyperaldosteronism
high BP
muscle weakness
polyuria
thirst
what is Liddle’s syndrome
inherited disease of high BP
cause of Liddle’s syndrome
mutation in aldosterone activated sodium channel and the channel is always on
results of Liddle’s syndrome
Na retention
hypertension
which parts have high baroreceptor conc (3)
carotid sinus
aortic arch
JGA
how low pressure side detect reduced in BP and counteract
low pressure
reduced baroreceptor firing
signal through afferent fibres to brainstem
SNS and ADH release
how low pressure side detect increase in BP and counteract
high pressure
atrial stretch
ANP and BNP release
how high pressure side detect reduced in BP and counteract
reduce BP
reudced baroreceptor firing
a) signal thru affernet fibres to brainstem to stimualte SNS and ADH release
b) stimulate JGA cells and release renin
when are ANP and BNP released
in respond to atrial stretch and high BP
actions of ANP
vasodilation of renal blood vessels
inhibit Na reabsorption in PCT and CT
inhibit release of renin and aldosterone
reduce BP
what are the direct effects of ACEi
reduce angiotensin ll
vascular effects of ACEi
vasodilation
increase vascular volume
reduce BP
reduce water reabsorption
direct renal effects of ACEi
reduce Na uptake in PCT
increase Na in distal nephron
adrenal effects of ACEi
reduce aldosterone
indirect renal effects of ACEi
reduce Na uptake in cortical CT
increase Na in distal nephron
where does loop diuretics act on
thick ascending LOH
where does thiazides diuretics act on
DCT
mechanism of carbonic anhydrase inhibitors
inhibit H2O+CO2 –> H2CO3
reduce Na reuptake in PCT
increase Na in distal nephron
reduce water reabsorption
effects of carbonic anhydrase inhibitors
increase urinary acidity
reduced Na+ reabsorption
example of loop diuretics
furosemide
mechanism of furosemide
triple transporter inhibitor
reduce Na reuptake in LOH
increase a in distal nephron
reduce water reabsorption
mechanism of thiazides
block Na+ Cl- uptake transporter
reduce Na+ reuptake in DCT
increase Na+ in distal nephron
increase Ca2+ reabsorption
reduce water reabsorption
mechanism of Potassium sparing diuretics
inhibits aldosterone function
example of potassium sparing diuretics
spironolactone
what is the main intracellular ion
K+
is K+ high or low in ECF
low
what is K+ uptake stimulated by after meal
insulin and aldosterone and adrenaline
what is K+ secretion stimulated by
aldosterone
increase tubular flow
increase plasma pH
increase [K+]
what cells secrete K+
principal cells
in principal cells what is the mechanism of K+ secretion
Na+ K+ ATPase uptake K+ and secrete Na+
K+ secretes out via K+ channel
causes of hypokalaemia
diet (too many processed food)
duretics
surreptitious vomiting
diarrhoea
genetics (mutation in Na/Cl transporter in distal nephron)
where is water reabsorped
PCT
descending limb of LOH
collecting duct
what is countercurrent multiplication
used to concentrate urine in the kidneys by the nephrons of the human excretory system.
most concetrated at bottom of LOH
where are UT-A2 found in nephron
think descedning LOH
where are UT-A1 and UT-A3 found in nephron
inner medullary collecting duct
UT-A1: apical membrane
UT-A3: basolateral membrane
what increases UT-A1 and UT-A3 numbers
vasopressin
role of UT-A2
transports urea across the apical membrane into the luminal space of cells in the thin descending loop of Henle of the kidneys.
role of UT-A1
urinary concentrating mechanism
what are the roles of urea transporter
facilitate urea reabsorption and concentration in the interstitium
what stimulates ADH production and release
increased plasma osmolarity
hypovolemia
decreased BP
nausea
angiotensin ll
nicotine
what inhibits ADH production and release
decreased plasma osmolarity
hypervolemia
increased BP
ethanol
ANP
mechanism of action of ADH
ADH release into blood vessels
bind to V2 receptor + G protein
cause adenylate cyclase to turn ATP to cAMP
cAMP + protein kinase A stimulates aquaporein 2 to insert onto membrane of collecting duct
what is diuresis
increased dilute urine excretion
where hv isomotic fluid
PCT
as excreted equal water and NaCl
where hv hypoosmotic fluid
end of LOH
which transporter helps with NaCl reabsorption at thick ascending LOH
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
K+Cl- symporter (K+ and Cl- out)
apical membrane:
Na+K+2Cl- symporter (Na, K, 2Cl in)
K+ channel (K+ out)
where has NaCl reabsorption
thick ascending LOH
DCT
which transporter helps with NaCl reabsorption at DCT
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
K+Cl- symporter (K+ and Cl- out)
apical membrane:
Na+Cl-symporter (Na and Cl in)
where is principal cells
collecting duct
which transporter helps with Na reabsorption at collecting duct
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
apical membrane:
Na+transporter (Na in)
where does ADH support Na+ reabsorption (3)
- thick ascedning limb (increase Na+ K+2 Cl- symporter)
- DCT (increase Na+ Cl- symporter)
- Collecting duct increase Na+ channel)
what is central diabetes insipidus
decreased production and release of ADH
clinical features of Central Diabetes insipidus
polyuria
polydipsia
treatment for central diabetes insipidus
extrenal ADH
what is Syndrome of Inappropriate ADH syndrome (SIADH)
increased production and release of ADH
clinical features of SIADH
hyperosmolar urine
hypervolemia
hyponatramia
treatment of SIADH
non peptude inhibitor of ADH
what is nephron diabetes insipidus
less or mutant AQP2
mutant V2 receptor
clinical features of nephron diabetes insipidus
polyuria
polydipsia
treatment for nephron diabetes insipidus
thiazide diuretics and NSAIDs
role of kidney for acid-base balance
secretion and excretion of H+
reabsorption of HCO3-
production of new HCO3-
where do we have reabsorption of HCO3- (4)
PCT (main)
thick ascending LOH
DCT
collecting duct
how reabsorption of HCO3- works at PCT
Na+HCO3- symporter
role of alpha intercalated cell at DCT and CT
HCO3- reabsorption
H+ secretion
role of Beta intercalated cell at DCT and CT
HCO3- secretion
H+ reabsorption
how alpha intercalated cells at DCT and CT healp HCO3- reabsorption
and H+ secretion
Cl-HCO3- antiporter at basolateral : HCO3- reabsorption
H+ATPase and H+K+ATPase and apical: H+ secretion
how beta intercalated cells at DCT and CT healp HCO3-secretion
and H+ reabsorption
H+ATPase at basolateral : H+ reabsorption
Cl-HCO3- antiporter at apical: HCO3- secretion
where does new bicarbonate production occur (3)
PCT
DCT
CT
which transporter helps production of bicarbonate at PCT
Na+ H+ antiporter
which transporter helps production of bicarbonate at DCT and CT
at alpha intercalated cells
H+ATPase, H+K+ATPase at apical
Cl-HCO3- antiporter at basolateral
what is metabolic acidosis
lowered [HCO3-]
compensatory response for metabolic acidosis
increase ventilation
increase [HCO3-] reabsorption and production
what is metabolic alkalosis
increase [HCO3-]
compensatory response for metabolic alkalosis
decrease ventilation
increase [HCO3-] excretion
what is respiratory acidosis
increase PCO2
compensatory response for respiratory acidosis
increase [HCO3-] reabsorption and production
what is respiratory alkalosis
reduce PCO2
compensatory response for respiratory alkalosis
reduce [HCO3-] reabsorption and production
which diuretic result in a higher osmolarity (loop or thiazide)
thiazide
where does loop diuretic act on
thick ascending LOH
where does thiazide act on
DCT
what are the 2 types of haematuria
- microscopic
- macroscopic
what is the most common kidney cancer
renal cell carcinoma (adenocarcinoma)
commonest type of renal cell carcinoma
clear cell
followed by papillary then chromophobe renal cell
risk factor of kidney cancer
old age
smoking
obesity
high BP
Hep C
inherited syndrome
treatment for kidney failure
investigations for painless visible haematuria in kidney cancer
flexible cystoscopy
CT urogram
renal function
investigations for persistent non visible haematuria in kidney cancer
flexible cystoscopy
US KUB
investigations for suspected kidney cancer
CT renal triple phase
staging CT chest
bone scan if symptomatic
what are the staging and grading for kidney cancer
TNM (T1-4), (N1-2), (M0-1)
Fuhrman grade (1-4) (is it well differentiated or what)
how to treat patient with small tumors unfit for surgery
cryosurgery
management for kidney cancer in general
laparoscopy
partial nephrectomy
radical nephrectomy
management for metastatic disease in kidney cancer
receptor tyrosine kinase inhibitors
immunotherapy
what are red flags of kidney cancer
painless haematuria
persistent microscopic haematuria
features of kidney cancer
haemoptysis
loin pain
palpable mass
metastatic disease (eg bones)
red flags of bladder cancer
painless haematuria
persistent microscopic haematuria
features of bladder cancer
suprapubic pain
lower urinary tract symptoms
UTI
metastatic disease symptoms
lower limb swelling
investigations for painless visible haematuria in bladder cancer
flexible cystoscopy
CT urogram
Renal function test
investigations forpersistent microscopic haematuria in bladder cancer
flexible cystoscopy
US KUB
what is transurethral resection of bladder lesion mean
uses heat to cut put all visible bladder tumor
provide histology and can be curative
after taking biopsy of suspected kidney/bladder cancer, what to decide
whether it is invasive or not then to decide treatment
what is the management protocol for non muscle invasive bladder cancer
if low grade and no CIS consider cystoscopic surveillance with or without intravesicular chemo / BCG(immunotherapy)
what is the management protocol for muscle invasive bladder cancer
cystectomy
radiotherapy
+/- chemo
palliative
what is ureteric TCC
ureteric transitional cell carcinoma
can block kidney
what type of cancer is prostate cancer
adenocarcinoma
risk factor of prostate cancer
age
western nations (scandinavian countries)
ethnicity (african americans)
what type of cancer is kidney cancer
renal cell carcinoma
what type of cancer is bladder cancer
transitional cell carcinoma
risk factor of prostate cancer
age
ethnic grp
family history obesity
diet
what is PSA and where is it produced
prostate specific antigen
produced by glandular tissue of prostate
produced at detectable levels only by prostate tissues
when will PSA level increase
trauma
infection / UTI
benign enlargement (benign prostatic hyperplasia)
prostate cancer
does prostate enlarge with age
yes
blood tests for prostate cancer
PSA
imaging for prostate cancer
MRI
benefits of trans perineal prostate biopsy
less risk of infection
can sample all areas of prostate
which biopsy is used for prostate cancer
trans perineal prostate biopsy
staging and grading for prostate cancer
TNM
Gleason score
staging and grading of bladder cancer
TNM
WHO classification
what does prostate cancer management highly depend on (4)
patient age, comorbidities
stage and grade of cancer
management for young + fit + high grade prostate cancer
radical prostectomy / radiotherapy / focal
management for young + fit + low grade prostate cancer
active surveillance (regular PSA, MRI, biopsy)
management for old+ unfit + high grade cancer / metastatic disease
hormone therapy
management for old+ unfit + low grade cancer / metastatic disease
regular PSA testing
watchful waiting
prostatectomy side effects of prostate cancer
changes urethral length as removes the proximal urethral sphincter
risk of damage cavernous nerves causing erectile dysfunction
what does cavernous nerve innervate
bladder
urethra
is PSA specific to prostate cancer
no
it is prostate specific tho
which 2 components are main key to diagnose kidney failure
elevated plasma urea and creatinine
biochem findings in kidney failure
hyperkalaemia
hyponatraemia
metabolic acidosis
anaemia
why kidney failure usually lead to hypertension
kidney failure tends to reduce salt and water secretion
cause HTN and oedema, pulmonary oedema
how is hypovolemia related to AKI
salt and water loss in tubulointerstitial disorders causing damage to concentrating mechanism
hypovolemia cause AKI
Reduced blood flow to the kidneys can interfere with the kidney’s ability to filter blood
does acidosis related to hypo or hyperkalaemia
hyper
as H+ goes into cells and psuh K+ out into bloodstream
causes of hyperkalaemia in kidney failure
reduce K+ secretion in DCT from blood to tubular lumen
acidosis
symptoms of chronic kidney failure hyperkalaemia
cardiac arrhythmia
neural and muscular activity
vomiting
ECG changes in hyperkalaemia
peaked T waves
P wave: reduced amplitude, broadened, disappears
QRS: widened
heart block
asystole
why kidney failure related to anaemia
reduced erythropoietin
how kidney failure reduce 1-25 Vit D levels affect metabolism
reduced intestinal calcium absorption
hypocalcaemia
hyperparathyroidism to try compensate reduced in calcium
what risk does kidney failure have
cardiovascular risk
–> increased production of the hormones that control blood pressure, leading to high blood pressure (hypertension)
what are the cardiovascular risks that may result from kidney failure
HTN
diabetes
lipid abnormalities
vascular calcification (due to increase calcium phosphate)
non cardiovascular risks from kidney failure
inflammation
oxidative stress
mineral bone/ bone metabolism disorder
how to treat hypovolaemic in kidney failure
give fluids
how to treat hypervolaemic in kidney failure
diuretics
dialysis (if they cannot pee)
how to diagnose hyperkalaemia
look at ecg (tall tented t waves)
how to treat hyperkalaemia in kidney failure
- drive into cells (use sodium bicarbonate/ insulin dextrose)
- drive put of body (diuretics/dialysis)
- gut absorption (potassium binders)
what are some kidney failure long term management
haemodialysis
peritoneal dialysis
transplantation
in which kidney disease do we use end stage failure risk assessment
CKD
(not for acute)
conservative treatment for long term management in kidney failure
erythropoietin injections to correct anaemia
diuretics to correct salt water overload
phosphate binders
1-25 vit D supplements
what does the kidney failure risk equation (KFRE) composed of (4)
age
sex
CKD-EPI eGFR
urine albumin creatinine ratio (ACR)
why we avoid transfusions in transplantable patients with kidney disease
likely to reach end stage failure
how to assess GFR (5)
urea
creatinine
creatinine clearance
inulin clearance
radionuclide studies
disadvantages of using urea to assess GFR
poor indicator
confounded by diet,catabolic state, GI bleeding, drugs, liver function
disadvantages of using creatinine to assess GFR
affected by muscle mass, age, race, sex
most helpful out of all
disadvantages of using creatinine clearance to assess GFR
difficult for elderly to collect accurate sample
overestimation as small amount of creatinine is secreted into urine
benefits of in centre haemodialysis
3 times a week compared to home 5-7 times
what are drawbacks of haemodialysis
strict dietary constraints and salt/water intake restrictions
drawbacks of peritoneal dialysis
7 days a week (can hv a day off sometimes)
overnight
high chance of infection due to catheter or peritonitis
benefits of peritoneal dialysis
can travel easily
lesser constraints in food and water intake
can be done everywhere
what is a horseshoe kidney
2 kidneys joined tgt
what are the possible constriction points in ureter (3)
- pelvic ureteric junction (PUJ) (where renal pelvis join top of ureter)
- pelvic brim, cross the iliac vessels
- uretero-vescial junction (where ureter pass thru bladder wall)
when external urethral sphincter contract do we pee or not pee
not pee
which nervous system supply urinary bladder
ANS
artery supply of urinary bladder
superior and inferior vesical branches of internal iliac artery
drainage of urinary bladder
vesical plexus which drains into internal iliac vein
what is special abt urothelium of urinary bladder
a transitional epithelium
water proof
can cope with changes in volume without losing waterproof characteristics
blood supply of female urinary tract
internal pudendal arteries and external urethral meatus in vaginal vestibule
lymphatics of female urinary tract
proximal urethra into internal iliac nodes
distal urethra to superficial inguinal lymph nodes
nerve supply of female urinary tract
vesical plexus (proximal)
pudendal nerve (distal)
blood supply of male urinary tract prostate(3)
inferior vesical artery
urethra bulbourethral artery
internal pudendal artery
lymphatics of male urinary tract
prostatic and membranous urethra drain to obturator and internal iliac nodes
spongy urethra to deep and superficial inguinal nodes
nerve supply of male urinary tract
vesical plexus (proximal)
pudendal nerve (distal)
2 modes of bladder in micturition cycle
storage
voiding
which part of brain and brainstem control micturition
brain — prefrontal cortex
brainstem — pontine micturition centre
how does prefrontal cortex and pontine micturition centre control micturition
prefrontal cortex permits pontine micturition centre to change from storage mode to voiding
which nervous system activate bladder contraction
PNS
which nucleus cause sphincter relaxation in micturition
Onuf’s nucleus
which nervous system cause internal sphincter to contract
SNS
role of periaqueductal gray (PAG) in micturition
receives sensory info from viscera (eg bladder full) and decide what goes to cortex
role of Pontine micturition centre (PMC)
co-ordinates spinal centres, switch storage to voiding if permitted
which nervous system suppress bladder activity
SNS
what does SNS nerve innervate in pelvic organ
kidney
bladder
testicle
ureter
what does PNS nerve innervate in pelvic organ
bladder
what does pudendal nerve innervate in pelvic organ
penis
vaginal vestibule/clitoris
what are the autonomic receptor drug targets at bladder neck
alpha-adrenergic (a1)-alpha blocker
what are the autonomic receptor drug targets at detrusor
cholinergic M3/M2
Beta-adrenergic B-3 agonist
what are the autonomic receptor drug targets at erectile
nitrergic
risk factor of stress urinary incontinence
ageing
obesity
smoking
pregnancy
pathology of urinary incontinence (3)
impaired bladder
impaired urethral support
impaired urethral closure
what test to see urinary incontinence
urodynamic test
management for stress urinary incontinence
non-surgical: Physiotherapist to teach pelvic floor muscle exercise
surgical: place a sling to support urethra, using anterior vaginal wall to support urethra (colposuspension), periurethral bulking injection
what is overactive bladder (urgency or with urgency incontinence)
urinary urgency usually with urinary frequency and nocturia, with or w/o urgency urinary incontinence
risk factor of urinary urgency
age
prolapse
increased BMI
caffeine, nicotine (irritants)
symptoms of overactive bladder
nocturia
urgency incontinence, frequency
impact on QoL due to sleep disruption
anxiety and depression
male enlarge prostate and prolapse in women
investigations of overactive bladder
bladder diary
bladder scan
urodynamics
exclude infection with urine dip
management of overactive bladder
lifestyle changes
bladder retaining
neuromodulation
antimuscarinic drug
beta-3 agonist
what is benign prostatic hyperplasia
non malignant growth of prostate tissue
outward enlargement can be felt with rectal exam
risk factors of benign prostatic hyperplasia
hormonal effects of testosterone on prostate tissue
why benign prostatic hyperplasia can suppress urine flow
prostate enlargement can compress urethra, lead to reduction in urinary stream
pathology of benign prostatic hyperplasia
hyperplasia of both lateral lobes and median lobe, cause compression of urethra and therefore cause bladder outflow obstruction
signs and symptoms of benign prostatic hyperplasia
hesitancy in starting urination
poor stream
dribbling post micturition
can present with acute retention
how to test for prostate cancer
raised PSA
investigations for benign prostatic hyperplasia
urine dipstick
culture
bladder diary
urodynamic test
PSA in bloods
cystoscopy for bladder cancer
imaging for benign prostatic hyperplasia
USS to assess upper renal tracts
lifestyle management for benign prostatic hyperplasia
weight loss
reduce caffeine
fluid intake in evening
medical management for benign prostatic hyperplasia (2)
- a-blocker for prostate stromal smooth muscle and bladder neck, block to relax muscle tone
- 5-alpha reductase inhibitor to prevent conversion of testosterone into di-hydro-testosterone which promtoes prostate growth to result in shrinkage
surgery management for benign prostatic hyperplasia
transurethral resection of prostate (TURP)
