Urology and renal Flashcards
1
Q
what are the mechanisms to regulate sodium intake (2)
A
central
peripheral
2
Q
how central mechanism regulate sodium intake
A
- increase appeptite for na+
- lateral parabrachial nucleus suppress desire for Na+ intake
- euvolemia
- inhibition of Na+ intake by serotonin glutamate
3
Q
how peripheral mechanism regulate sodium intake
A
taste
4
Q
where is sodium reabsorbed in nephron
A
PCT
thick ascending limb
DCT
collecting duct
5
Q
what happens when there is increased tubular sodium and GFR
A
- 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
6
Q
role of juxtaglomerular cells
A
secrete renin
7
Q
how increased SNS activity control sodium excretion
A
increased reabsorption at collecting duct, PCT, LOH, DCT
reduce GFR rate
stimulate JGA produce more renin
8
Q
how Angiotensin ll control sodium excretion
A
increased reabsorption at PCT
increase aldosterone from adrenal gland to increase reabsorption at collecting duct
9
Q
what is the main vasodilator to control sodium excretion
A
atrial naturietic peptide (ANP)
10
Q
ANP role on decrease Na reabsorption
A
inhibit PCT, LOH, JGA, DCT, CT
11
Q
when low sodium, will there be more angiotensin l or less
A
more
12
Q
when low sodium, will there be more vasoconstriction or less
A
more
13
Q
where is aldosterone made and released
A
adrenal cortex zona glomerulosa
14
Q
what is aldosterone release in response to
A
angiotensin ll when decrease in BP via baroreceptors
15
Q
function of aldosterone for ions (3)
A
increase Na reabsorption
increase K+ secretion
increase H+ secretion
16
Q
what happens when aldosterone excess
A
hypokalaemic alkalosis
17
Q
why steroid can pass through membrane
A
steroid hormone
lipid soluble
18
Q
how aldosterone work in cells
A
aldosterone bind to mineralcorticoid receptor
translocate into nucleus
then bind to DNA for transcription
19
Q
what happens when aldosterone increase in cortical collecting duct
A
increase active na+ channel
20
Q
what happens in hypoaldosteronism
A
reduced Na reabsorption in distal nephron
increase urinary Na+ loss
ECF volume falls
increased renin and angiotensin ll and ADH
21
Q
symptoms of hypoaldosteronism
A
dizzy
low BP
salt craving
palpitations
22
Q
what happens in hyperaldosteronism
A
increased reabsorption of Na in distal nephron
reduced Na urinary loss
ECF volume increases
reduced renin, angiontensin ll and ADH
increase ANP, BNP
23
Q
what increases in hyperaldosterone
A
BP
ANP
BNP
24
Q
symptoms of hyperaldosteronism
A
high BP
muscle weakness
polyuria
thirst
25
what is Liddle's syndrome
inherited disease of high BP
26
cause of Liddle's syndrome
mutation in aldosterone activated sodium channel and the channel is always on
27
results of Liddle's syndrome
Na retention
hypertension
28
which parts have high baroreceptor conc (3)
carotid sinus
aortic arch
JGA
29
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
30
how low pressure side detect increase in BP and counteract
high pressure
atrial stretch
ANP and BNP release
31
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
32
when are ANP and BNP released
in respond to atrial stretch and high BP
33
actions of ANP
vasodilation of renal blood vessels
inhibit Na reabsorption in PCT and CT
inhibit release of renin and aldosterone
reduce BP
34
what are the direct effects of ACEi
reduce angiotensin ll
35
vascular effects of ACEi
vasodilation
increase vascular volume
reduce BP
reduce water reabsorption
36
direct renal effects of ACEi
reduce Na uptake in PCT
increase Na in distal nephron
37
adrenal effects of ACEi
reduce aldosterone
38
indirect renal effects of ACEi
reduce Na uptake in cortical CT
increase Na in distal nephron
39
where does loop diuretics act on
thick ascending LOH
40
where does thiazides diuretics act on
DCT
41
mechanism of carbonic anhydrase inhibitors
inhibit H2O+CO2 --> H2CO3
reduce Na reuptake in PCT
increase Na in distal nephron
reduce water reabsorption
42
effects of carbonic anhydrase inhibitors
increase urinary acidity
reduced Na+ reabsorption
43
example of loop diuretics
furosemide
44
mechanism of furosemide
triple transporter inhibitor
reduce Na reuptake in LOH
increase a in distal nephron
reduce water reabsorption
45
mechanism of thiazides
block Na+ Cl- uptake transporter
reduce Na+ reuptake in DCT
increase Na+ in distal nephron
increase Ca2+ reabsorption
reduce water reabsorption
46
mechanism of Potassium sparing diuretics
inhibits aldosterone function
47
example of potassium sparing diuretics
spironolactone
48
what is the main intracellular ion
K+
49
is K+ high or low in ECF
low
50
what is K+ uptake stimulated by after meal
insulin and aldosterone and adrenaline
51
what is K+ secretion stimulated by
aldosterone
increase tubular flow
increase plasma pH
increase [K+]
52
what cells secrete K+
principal cells
53
in principal cells what is the mechanism of K+ secretion
Na+ K+ ATPase uptake K+ and secrete Na+
K+ secretes out via K+ channel
54
causes of hypokalaemia
diet (too many processed food)
duretics
surreptitious vomiting
diarrhoea
genetics (mutation in Na/Cl transporter in distal nephron)
55
where is water reabsorped
PCT
descending limb of LOH
collecting duct
56
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
57
where are UT-A2 found in nephron
think descedning LOH
58
where are UT-A1 and UT-A3 found in nephron
inner medullary collecting duct
UT-A1: apical membrane
UT-A3: basolateral membrane
59
what increases UT-A1 and UT-A3 numbers
vasopressin
60
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.
61
role of UT-A1
urinary concentrating mechanism
62
what are the roles of urea transporter
facilitate urea reabsorption and concentration in the interstitium
63
what stimulates ADH production and release
increased plasma osmolarity
hypovolemia
decreased BP
nausea
angiotensin ll
nicotine
64
what inhibits ADH production and release
decreased plasma osmolarity
hypervolemia
increased BP
ethanol
ANP
65
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
66
what is diuresis
increased dilute urine excretion
67
where hv isomotic fluid
PCT
as excreted equal water and NaCl
68
where hv hypoosmotic fluid
end of LOH
69
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)
70
where has NaCl reabsorption
thick ascending LOH
DCT
71
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)
72
where is principal cells
collecting duct
73
which transporter helps with Na reabsorption at collecting duct
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
apical membrane:
Na+transporter (Na in)
74
where does ADH support Na+ reabsorption (3)
1. thick ascedning limb (increase Na+ K+2 Cl- symporter)
2. DCT (increase Na+ Cl- symporter)
3. Collecting duct increase Na+ channel)
75
what is central diabetes insipidus
decreased production and release of ADH
76
clinical features of Central Diabetes insipidus
polyuria
polydipsia
77
treatment for central diabetes insipidus
extrenal ADH
78
what is Syndrome of Inappropriate ADH syndrome (SIADH)
increased production and release of ADH
79
clinical features of SIADH
hyperosmolar urine
hypervolemia
hyponatramia
80
treatment of SIADH
non peptude inhibitor of ADH
81
what is nephron diabetes insipidus
less or mutant AQP2
mutant V2 receptor
82
clinical features of nephron diabetes insipidus
polyuria
polydipsia
83
treatment for nephron diabetes insipidus
thiazide diuretics and NSAIDs
84
role of kidney for acid-base balance
secretion and excretion of H+
reabsorption of HCO3-
production of new HCO3-
85
where do we have reabsorption of HCO3- (4)
PCT (main)
thick ascending LOH
DCT
collecting duct
86
how reabsorption of HCO3- works at PCT
Na+HCO3- symporter
87
role of alpha intercalated cell at DCT and CT
HCO3- reabsorption
H+ secretion
88
role of Beta intercalated cell at DCT and CT
HCO3- secretion
H+ reabsorption
89
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
90
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
91
where does new bicarbonate production occur (3)
PCT
DCT
CT
92
which transporter helps production of bicarbonate at PCT
Na+ H+ antiporter
93
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
94
what is metabolic acidosis
lowered [HCO3-]
95
compensatory response for metabolic acidosis
increase ventilation
increase [HCO3-] reabsorption and production
96
what is metabolic alkalosis
increase [HCO3-]
97
compensatory response for metabolic alkalosis
decrease ventilation
increase [HCO3-] excretion
98
what is respiratory acidosis
increase PCO2
99
compensatory response for respiratory acidosis
increase [HCO3-] reabsorption and production
100
what is respiratory alkalosis
reduce PCO2
101
compensatory response for respiratory alkalosis
reduce [HCO3-] reabsorption and production
102
which diuretic result in a higher osmolarity (loop or thiazide)
thiazide
103
where does loop diuretic act on
thick ascending LOH
104
where does thiazide act on
DCT
105
what are the 2 types of haematuria
1. microscopic
2. macroscopic
106
what is the most common kidney cancer
renal cell carcinoma (adenocarcinoma)
107
commonest type of renal cell carcinoma
clear cell
followed by papillary then chromophobe renal cell
108
risk factor of kidney cancer
old age
smoking
obesity
high BP
Hep C
inherited syndrome
treatment for kidney failure
109
investigations for painless visible haematuria in kidney cancer
flexible cystoscopy
CT urogram
renal function
110
investigations for persistent non visible haematuria in kidney cancer
flexible cystoscopy
US KUB
111
investigations for suspected kidney cancer
CT renal triple phase
staging CT chest
bone scan if symptomatic
112
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)
113
how to treat patient with small tumors unfit for surgery
cryosurgery
114
management for kidney cancer in general
laparoscopy
partial nephrectomy
radical nephrectomy
115
management for metastatic disease in kidney cancer
receptor tyrosine kinase inhibitors
immunotherapy
116
what are red flags of kidney cancer
painless haematuria
persistent microscopic haematuria
117
features of kidney cancer
haemoptysis
loin pain
palpable mass
metastatic disease (eg bones)
118
red flags of bladder cancer
painless haematuria
persistent microscopic haematuria
119
features of bladder cancer
suprapubic pain
lower urinary tract symptoms
UTI
metastatic disease symptoms
lower limb swelling
120
investigations for painless visible haematuria in bladder cancer
flexible cystoscopy
CT urogram
Renal function test
121
investigations forpersistent microscopic haematuria in bladder cancer
flexible cystoscopy
US KUB
122
what is transurethral resection of bladder lesion mean
uses heat to cut put all visible bladder tumor
provide histology and can be curative
123
after taking biopsy of suspected kidney/bladder cancer, what to decide
whether it is invasive or not then to decide treatment
124
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)
125
what is the management protocol for muscle invasive bladder cancer
cystectomy
radiotherapy
+/- chemo
palliative
126
what is ureteric TCC
ureteric transitional cell carcinoma
can block kidney
127
what type of cancer is prostate cancer
adenocarcinoma
128
risk factor of prostate cancer
age
western nations (scandinavian countries)
ethnicity (african americans)
129
what type of cancer is kidney cancer
renal cell carcinoma
130
what type of cancer is bladder cancer
transitional cell carcinoma
131
risk factor of prostate cancer
age
ethnic grp
family history obesity
diet
132
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
133
when will PSA level increase
trauma
infection / UTI
benign enlargement (benign prostatic hyperplasia)
prostate cancer
134
does prostate enlarge with age
yes
135
blood tests for prostate cancer
PSA
136
imaging for prostate cancer
MRI
137
benefits of trans perineal prostate biopsy
less risk of infection
can sample all areas of prostate
138
which biopsy is used for prostate cancer
trans perineal prostate biopsy
139
staging and grading for prostate cancer
TNM
Gleason score
140
staging and grading of bladder cancer
TNM
WHO classification
141
what does prostate cancer management highly depend on (4)
patient age, comorbidities
stage and grade of cancer
142
management for young + fit + high grade prostate cancer
radical prostectomy / radiotherapy / focal
143
management for young + fit + low grade prostate cancer
active surveillance (regular PSA, MRI, biopsy)
144
management for old+ unfit + high grade cancer / metastatic disease
hormone therapy
145
management for old+ unfit + low grade cancer / metastatic disease
regular PSA testing
watchful waiting
146
prostatectomy side effects of prostate cancer
changes urethral length as removes the proximal urethral sphincter
risk of damage cavernous nerves causing erectile dysfunction
147
what does cavernous nerve innervate
bladder
urethra
148
is PSA specific to prostate cancer
no
it is prostate specific tho
149
which 2 components are main key to diagnose kidney failure
elevated plasma urea and creatinine
150
biochem findings in kidney failure
hyperkalaemia
hyponatraemia
metabolic acidosis
anaemia
151
why kidney failure usually lead to hypertension
kidney failure tends to reduce salt and water secretion
cause HTN and oedema, pulmonary oedema
152
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
153
does acidosis related to hypo or hyperkalaemia
hyper
as H+ goes into cells and psuh K+ out into bloodstream
154
causes of hyperkalaemia in kidney failure
reduce K+ secretion in DCT from blood to tubular lumen
acidosis
155
symptoms of chronic kidney failure hyperkalaemia
cardiac arrhythmia
neural and muscular activity
vomiting
156
ECG changes in hyperkalaemia
peaked T waves
P wave: reduced amplitude, broadened, disappears
QRS: widened
heart block
asystole
157
why kidney failure related to anaemia
reduced erythropoietin
158
how kidney failure reduce 1-25 Vit D levels affect metabolism
reduced intestinal calcium absorption
hypocalcaemia
hyperparathyroidism to try compensate reduced in calcium
159
what risk does kidney failure have
cardiovascular risk
--> increased production of the hormones that control blood pressure, leading to high blood pressure (hypertension)
160
what are the cardiovascular risks that may result from kidney failure
HTN
diabetes
lipid abnormalities
vascular calcification (due to increase calcium phosphate)
161
non cardiovascular risks from kidney failure
inflammation
oxidative stress
mineral bone/ bone metabolism disorder
162
how to treat hypovolaemic in kidney failure
give fluids
163
how to treat hypervolaemic in kidney failure
diuretics
dialysis (if they cannot pee)
164
how to diagnose hyperkalaemia
look at ecg (tall tented t waves)
165
how to treat hyperkalaemia in kidney failure
1. drive into cells (use sodium bicarbonate/ insulin dextrose)
2. drive put of body (diuretics/dialysis)
3. gut absorption (potassium binders)
166
what are some kidney failure long term management
haemodialysis
peritoneal dialysis
transplantation
167
in which kidney disease do we use end stage failure risk assessment
CKD
(not for acute)
168
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
169
what does the kidney failure risk equation (KFRE) composed of (4)
age
sex
CKD-EPI eGFR
urine albumin creatinine ratio (ACR)
170
why we avoid transfusions in transplantable patients with kidney disease
likely to reach end stage failure
171
how to assess GFR (5)
urea
creatinine
creatinine clearance
inulin clearance
radionuclide studies
172
disadvantages of using urea to assess GFR
poor indicator
confounded by diet,catabolic state, GI bleeding, drugs, liver function
173
disadvantages of using creatinine to assess GFR
affected by muscle mass, age, race, sex
most helpful out of all
174
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
175
benefits of in centre haemodialysis
3 times a week compared to home 5-7 times
176
what are drawbacks of haemodialysis
strict dietary constraints and salt/water intake restrictions
177
drawbacks of peritoneal dialysis
7 days a week (can hv a day off sometimes)
overnight
high chance of infection due to catheter or peritonitis
178
benefits of peritoneal dialysis
can travel easily
lesser constraints in food and water intake
can be done everywhere
179
what is a horseshoe kidney
2 kidneys joined tgt
180
what are the possible constriction points in ureter (3)
1. pelvic ureteric junction (PUJ) (where renal pelvis join top of ureter)
2. pelvic brim, cross the iliac vessels
3. uretero-vescial junction (where ureter pass thru bladder wall)
181
when external urethral sphincter contract do we pee or not pee
not pee
182
which nervous system supply urinary bladder
ANS
183
artery supply of urinary bladder
superior and inferior vesical branches of internal iliac artery
184
drainage of urinary bladder
vesical plexus which drains into internal iliac vein
185
what is special abt urothelium of urinary bladder
a transitional epithelium
water proof
can cope with changes in volume without losing waterproof characteristics
186
blood supply of female urinary tract
internal pudendal arteries and external urethral meatus in vaginal vestibule
187
lymphatics of female urinary tract
proximal urethra into internal iliac nodes
distal urethra to superficial inguinal lymph nodes
188
nerve supply of female urinary tract
vesical plexus (proximal)
pudendal nerve (distal)
189
blood supply of male urinary tract prostate(3)
inferior vesical artery
urethra bulbourethral artery
internal pudendal artery
190
lymphatics of male urinary tract
prostatic and membranous urethra drain to obturator and internal iliac nodes
spongy urethra to deep and superficial inguinal nodes
191
nerve supply of male urinary tract
vesical plexus (proximal)
pudendal nerve (distal)
192
2 modes of bladder in micturition cycle
storage
voiding
193
which part of brain and brainstem control micturition
brain --- prefrontal cortex
brainstem --- pontine micturition centre
194
how does prefrontal cortex and pontine micturition centre control micturition
prefrontal cortex permits pontine micturition centre to change from storage mode to voiding
195
which nervous system activate bladder contraction
PNS
196
which nucleus cause sphincter relaxation in micturition
Onuf's nucleus
197
which nervous system cause internal sphincter to contract
SNS
198
role of periaqueductal gray (PAG) in micturition
receives sensory info from viscera (eg bladder full) and decide what goes to cortex
199
role of Pontine micturition centre (PMC)
co-ordinates spinal centres, switch storage to voiding if permitted
200
which nervous system suppress bladder activity
SNS
201
what does SNS nerve innervate in pelvic organ
kidney
bladder
testicle
ureter
202
what does PNS nerve innervate in pelvic organ
bladder
203
what does pudendal nerve innervate in pelvic organ
penis
vaginal vestibule/clitoris
204
what are the autonomic receptor drug targets at bladder neck
alpha-adrenergic (a1)-alpha blocker
205
what are the autonomic receptor drug targets at detrusor
cholinergic M3/M2
Beta-adrenergic B-3 agonist
206
what are the autonomic receptor drug targets at erectile
nitrergic
207
risk factor of stress urinary incontinence
ageing
obesity
smoking
pregnancy
208
pathology of urinary incontinence (3)
impaired bladder
impaired urethral support
impaired urethral closure
209
what test to see urinary incontinence
urodynamic test
210
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
211
what is overactive bladder (urgency or with urgency incontinence)
urinary urgency usually with urinary frequency and nocturia, with or w/o urgency urinary incontinence
212
risk factor of urinary urgency
age
prolapse
increased BMI
caffeine, nicotine (irritants)
213
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
214
investigations of overactive bladder
bladder diary
bladder scan
urodynamics
exclude infection with urine dip
215
management of overactive bladder
lifestyle changes
bladder retaining
neuromodulation
antimuscarinic drug
beta-3 agonist
216
what is benign prostatic hyperplasia
non malignant growth of prostate tissue
outward enlargement can be felt with rectal exam
217
risk factors of benign prostatic hyperplasia
hormonal effects of testosterone on prostate tissue
218
why benign prostatic hyperplasia can suppress urine flow
prostate enlargement can compress urethra, lead to reduction in urinary stream
219
pathology of benign prostatic hyperplasia
hyperplasia of both lateral lobes and median lobe, cause compression of urethra and therefore cause bladder outflow obstruction
220
signs and symptoms of benign prostatic hyperplasia
hesitancy in starting urination
poor stream
dribbling post micturition
can present with acute retention
221
how to test for prostate cancer
raised PSA
222
investigations for benign prostatic hyperplasia
urine dipstick
culture
bladder diary
urodynamic test
PSA in bloods
cystoscopy for bladder cancer
223
imaging for benign prostatic hyperplasia
USS to assess upper renal tracts
224
lifestyle management for benign prostatic hyperplasia
weight loss
reduce caffeine
fluid intake in evening
225
medical management for benign prostatic hyperplasia (2)
1. a-blocker for prostate stromal smooth muscle and bladder neck, block to relax muscle tone
2. 5-alpha reductase inhibitor to prevent conversion of testosterone into di-hydro-testosterone which promtoes prostate growth to result in shrinkage
226
surgery management for benign prostatic hyperplasia
transurethral resection of prostate (TURP)
227
228
