Urinary Flashcards
1
Q
order of blood vessels in
A
renal, segmental, interLOBAR, arcuate, interLOBULAR, afferent, efferent
2
Q
location of R and L kidneys
A
R- T12-L3
L- T11-L2
3
Q
why is lower kidney lower down
A
it is compressed by liver
4
Q
filtration fraction equaiton
A
amount filtered (GFR) / plasma flow (RPF)
5
Q
what is used to estimate GFR in children
A
51 CR EDTA
6
Q
what are the forces affecting glomerular filtration?
A
pGC, pBC, πGC
7
Q
which forces increase glomerular filtration
A
pGC
8
Q
which forces reduce glomerular filtration
A
pBC, πGC
9
Q
3 things that stimulate renin release
A
increasing SNS innervation, reduced stretch afferent, reduced NaCl at MD cells
10
Q
equation clearance
A
clearance(GFR) = concentration x flow rate / plasma concentration
11
Q
filtration rate
A
plasma concentration x GFR
12
Q
excretion rate
A
concentration x flow rate
13
Q
how many mg in a gram?
how many micrograms in a mg and a gram?
A
1000 mg in a gram
1000 micrograms in a mg
therefore 1,000,000 micrograms in a gram
14
Q
describe permeability of LoH in different sections
A
descending- permeable to H2O, Na and Cl
thin ascending- impermeable to water and Na/Cl
thick ascending- permeable to NaCl but not H2O
15
Q
what is the importance of urea
A
the maintained pool of urea in the medullary interstitial creates corticocapilalry gradient along with NaCL. this drives h2O resorption
16
Q
action of urea in DCT
A
inserts aquaporins and UT1 to increase water and urea resorption.
17
Q
3 things that cause renin release
A
increase in sympathetic stimulation, decrease in afferent arteriole stretch, decrease in NaCl at MD cells
18
Q
what starling forces would reduce NaCl absorption
A
reduction in pGC, increase in oncotic GC and pBC
19
Q
role of prostoglandins
A
increase renin release, and systemic vasodilation
20
Q
what does ADH do at V1 and V2 receptors
A
V1- vasoconstriction
V2- increase Aquaporins in CD
21
Q
role of ANP
A
released to increase in circulating volume
- reduces ENaC
- vasodilates afferent to increase
- inhibits aldosterone
- inhibits ADH
- decreases renin
22
Q
causes of fluid overload
A
hypoaldosteronism, excesive Na+ intake, cirrhosis, renal disease
23
Q
cause central DI
A
basilar skull fracture, sarcoidosis, tumour, aneurysm
24
Q
cause nephrogenic DI and how to manage
A
low protein, low salt diet
caused by mutation in V2 receptor, chronic pyelonephritis, polycystic kidney
25
cause SIADH
CNS disorders, lung diseases, drugs, hypothyroidism
26
what is hypernatraemia and what is its causes
plasma sodium above 146
osmotic diuresis, fluid loss eg. vomiting,D DI, primary aldosteronism.
27
what is hyponatraemia and what is its causes
serum Na lower than 135
diuretics, water overload, increased ADH, D and V, burns
28
symptoms hyponatraemia
agitation, nausea, focal neurology, coma
29
hypovolemic hyponatraemia vs hypervolaemic hyponatraemia
Hypovolemic hyponatremia: decrease in total body water with greater decrease in total body sodium
Hypervolemic hyponatremia: increase in total body sodium with greater increase in total body water
30
causes of hypovolaemic hyponatraemia
non renal
GI- vomiting
excessvie sweating
ascites
cerebral salt wasting solution
31
treatment hypovolaemic hyponatraemia
fluid restriction
32
ecg of hypo and hyperkalaemia
hypokalaemia- slightly peaked p wave, shallow t wave, prominent u wave
hyperkalaemia- wide flat p wave, tall peaked t wave, widened qrs
33
describe RMP for hypo/hyperkalaemia
hypo- rmp increased, cell hyperpolarised
hyper- rmp decreased, depolarised cell
34
symptoms hypo hyperkalaemia
hypo- muscle weakness, tetany, vasoconstriction, thirst due to impaired ash, metabolic alkalosis due to increased intracellular H+
hyper- muscle weakness, cardiac arrhythmias
35
treatment hyperkalaemia
calcium gluconate to stabilise myocardium
insulin to lower plasma K+
calcium resonium to reduce K+ in body
36
describe transport of k+ across nephron
PCT- solvent drag
LoH- NKCC
DT/CD- ROMK
37
apical transporters in proximal tubule
Na+ glutamate/AA/organic transporter
Na+H+ antiport (amiloride)
Cl- Base antiport
38
apical transporters ascending loop of henle
NaKCC (Loop diuretic)
ROMK
39
apical transporters distal tubule
NaCl (thiazide)
ENaC
Ca2+ uniport
40
apical transporters principal cell collecting duct
Aquaporins
ENaC
ROMK out
41
apical transportes in alpha intercalated cell
H+ out
K+H+ antiporter (K+ in)
42
apical transporters in beta intercalated cell
K+ out
Cl-HCO3- antiporter (Cl- in)
43
effects of alkalaemia
decreases free ions by causing Calcium ions to come out of solution, increasing neuronal excitability and firing of action potentials.
causes tetany, muscle twitches and numbness
44
effects of academia
increases free ions by causing calcium ions to enter solution. causes arrythmias
45
control of pH in PCT
46
alpha intercated cell
47
beta intercalated cell
48
how to calculate anion gap and what causes it
Na+ + K+ - CL- + HCO3-
if metabolic acid produced in metabolic acidosis this reacts with HCO3- and reduces HCO3- levels. this causes anion gap to increase
49
what causes metabolic alkalosis
excessive vomiting
50
pre renal causes of AKI
hypovolaemia, shock (septic, hypovolaemia,cardiogenic), ischaemia (NSAIDS pre G ACE post G), cardiac shock
51
renal causes of AKI
vasculitis
acute tubular nephritis- rhabdomyolytis and myoglobin causing ischemia
acute interstitial nephritis- nephrotoxic drugs
52
nephrotic syndrome triad and treatment
- oedema
- hypoablumenia
- protinurea \>350ml/mmol
treat hypertension, diuretics, ACEi
53
4 things causing nephrotic syndrome
diabetes, FSGS, membranous GN, minimal change GN
54
triad of neprhitic syndrome and treatment
- haematuria
- hypertension
- reduction in GFR
treat hypertension, manage CVS risk factors, steroids/immunosuppresants, oedema
55
4 things causing nephritic syndrome
goodpastures
IgA nephropathy
rapidly progressive GN
post streptococcal GN
56
how does CKD cause bone disease
reduced renal function
reduced Vit D resporption
reduced calcium
PTH released
bone resorption
57
2 types periotneal dialysis
APD, CAPD
58
treatment of CKD hyperkalaemia and acidosis
- oral NaHCO3 tablets
- reduce K+ intake, stop ACEi, avoid K+ increasing drugs
59
how to measure extend of CKD
G1-G5 measurs GFR
A1-A3 measures albumin in urine
60
which receptors mictruition
voiding (parasympathetic) M3
storage (sympathetic) B3, A1
61
investigations incontenence
cytoscopy, urodynamics, frequency volume, pad test, urine dipstick
62
medication incontenence
duloxetine- serotonin and NA inhibitor. increases IUS contraction
63
surgery incontenence
intramural bulking, mesh
male sling, artficial sphincter
64
describe development of urogenital sinus
the urorectal septum splits the cloaca into the urogenital sinus and anal canal
65
describe the derivatives of urogenital sinus
upper- bladder
pelvic part- entire urethra in females, and the prostatic and membranous urethra in males.
phallic/caudal part- spongy urethra in males.
66
what are the excretory and collecting sections of kidney formed from
excretory- intermediate mesoderm acted on by ureteric bud to form metanephric blastema.
collecting- ureteric bud
67
3 things that make kidney
pronephros
mesonephros
metanephros
68
formation of bladder in males
1. mesonephric duct reaches urogenital sinus (UGS)
2. mesonephric duct spouts ureteric bud
3. UGS expands
4. ureteric bud and mesoneprhric duct make independent openings in UGS
69
where do loop, thiazide and K+ sparing act and example of each
loop- LoH. inhibit NKCC. furesomide
thiazide- DCT. NaCl. bendroflumethiazide
K+- DCT, CD. block ENaC. amiloride/spironalactone
70
which conditions treated by loop diuretics
- Nephrotic syndrome
- Renal failure
- Cirrhosis of liver (spironolactone preferred)
- hyperkalaemia
- hypercalcaemia
71
use thiazide diuretics
hypertension
72
use aldosterone antagonists
- Reduces mortality in heart failure
- Preferred drug for cirrhosis (ascites & oedema)
- Additional therapy in hypertension caused by primary hyperaldosteronism
73
use ENaC blockers
Usually used in combination with K+ losing diuretics such as Loop or Thiazide diuretics to minimise K+loss
74
use carbonic anhyrase inhibitors
glaucoma
75
use osmotic diuresis
cerebral oedema
76
what antibiotic sumple UTI
rimethoprim or nitrofurantoin (3 day course)
77
treatment complicated UTI
Trimethoprim, nitrofurantoin or cephalexin (5-7 day course)
78
treatment pyelonephritis
- Co-amoxiclav (14 day course)
- Ciprofloxacin (effective as a 7 day course)
- Gentamicin (IV only – nephrotoxic)
79
2 most common bacteria in females
- e coli
- staphyloccus saprophyticus
80
RCC
- what is it
- risks
- presentation
- investigations
- treatments
- renal cell caricnoma of tubular epithelium
- obesity, smoking, dialysis
- haematuria/incidental findings. varicoele, hypercalcaemia
- radiology, endoscopy, urine cstology
- if localised, surevilance and nephrectomy
- if metastatic, pallitative care
81
TCC
- what is it
- risks
- presentation
- investigations
- treatments
- urothelial cell carcinoma(bladder)
- smoking, analine dyes
- incidental finding, haematuria, obstruction, wightloss
- diagnosed by TURBT, cytoscopy and biopsy
- low risk: TURBT and intravesile chemo
high risk non invasive: TURBT, intravesile chemo and BCG, cystectomy
high risk invasive: cystectomy, radiotherapy
82
TCC upper urinary tract
- haematuria and obsturction
- nephro-ureterectomy
83
most common renal carcinoa
RCC
84
risks polycystic kidney disease
- causes steadily progressive CKD and can cause subarachnoid haemorrage
- bleeding into cysts
85
simple cortical cysts vs polycystic kidney disease
simpel cortical cysts dont reduce kidney function
86
daily requirements
30ml/kg/day water
1mmol/kg/day Na+ K+ Cl-
50-100g day glucose
87
water %
baby 75%
elderly 45%
woman 50%
88
Mechanism osmotic duiresisp
Expands ECF volume initially, decreases blood viscosity, inhibit renin release, increase renal blood flow
89
Use osmotic diuretics
Acute renal failure due to shock, acute drug poisoning, reduce intracranial pressure
90
Side effects osmotic diuretics
Headache, nausea, vomiting (hyponatraemia). ECF expansion and so makes HF worse, dehydration and hypernatraemia
91
formation of bladder females
1. mesonephric duct reaches the UGS
2. mesonephric duct spouts ureteric bud
3. mesonephric duct regresses and UGS expands
4. ureteric bud opens into UGS
92
what does the mesonephros form in adults
the trigone
93
which pathogen
-ve nitrites
+ve leucocyte esterase
staphylococcus sapprophyticus
94
which pathogen
+ve nitries
+ve leucocyte esterase
e coli
95
treatment overactive bladder
antimuscarinic
96
treatment SUI
duloxetone
97
multiple myeloma signs
increased globulin, calcium, kidney size and recurrent infections
98
findings SLE
wire loop thickening
99
findings membranous glomerulonephritis
thickened capillary loop
100
ions in sweat
anion- cholide
cation- sodium
101
where do renal arteries originate
abdominal aorta, below SMA
