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ESA3 wrong answers > Urinary > Flashcards

Urinary Flashcards

1
Q

order of blood vessels in

A

renal, segmental, interLOBAR, arcuate, interLOBULAR, afferent, efferent

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2
Q

location of R and L kidneys

A

R- T12-L3
L- T11-L2

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3
Q

why is lower kidney lower down

A

it is compressed by liver

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4
Q

filtration fraction equaiton

A

amount filtered (GFR) / plasma flow (RPF)

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5
Q

what is used to estimate GFR in children

A

51 CR EDTA

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6
Q

what are the forces affecting glomerular filtration?

A

pGC, pBC, πGC

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7
Q

which forces increase glomerular filtration

A

pGC

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8
Q

which forces reduce glomerular filtration

A

pBC, πGC

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9
Q

3 things that stimulate renin release

A

increasing SNS innervation, reduced stretch afferent, reduced NaCl at MD cells

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10
Q

equation clearance

A

clearance(GFR) = concentration x flow rate / plasma concentration

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11
Q

filtration rate

A

plasma concentration x GFR

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12
Q

excretion rate

A

concentration x flow rate

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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

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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

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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

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16
Q

action of urea in DCT

A

inserts aquaporins and UT1 to increase water and urea resorption.

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17
Q

3 things that cause renin release

A

increase in sympathetic stimulation, decrease in afferent arteriole stretch, decrease in NaCl at MD cells

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18
Q

what starling forces would reduce NaCl absorption

A

reduction in pGC, increase in oncotic GC and pBC

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19
Q

role of prostoglandins

A

increase renin release, and systemic vasodilation

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20
Q

what does ADH do at V1 and V2 receptors

A

V1- vasoconstriction
V2- increase Aquaporins in CD

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21
Q

role of ANP

A

released to increase in circulating volume

  • reduces ENaC
  • vasodilates afferent to increase
  • inhibits aldosterone
  • inhibits ADH
  • decreases renin
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22
Q

causes of fluid overload

A

hypoaldosteronism, excesive Na+ intake, cirrhosis, renal disease

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23
Q

cause central DI

A

basilar skull fracture, sarcoidosis, tumour, aneurysm

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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

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25
Q

cause SIADH

A

CNS disorders, lung diseases, drugs, hypothyroidism

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26
Q

what is hypernatraemia and what is its causes

A

plasma sodium above 146

osmotic diuresis, fluid loss eg. vomiting,D DI, primary aldosteronism.

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27
Q

what is hyponatraemia and what is its causes

A

serum Na lower than 135

diuretics, water overload, increased ADH, D and V, burns

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28
Q

symptoms hyponatraemia

A

agitation, nausea, focal neurology, coma

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29
Q

hypovolemic hyponatraemia vs hypervolaemic hyponatraemia

A

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

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30
Q

causes of hypovolaemic hyponatraemia

A

non renal
GI- vomiting
excessvie sweating
ascites
cerebral salt wasting solution

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31
Q

treatment hypovolaemic hyponatraemia

A

fluid restriction

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32
Q

ecg of hypo and hyperkalaemia

A

hypokalaemia- slightly peaked p wave, shallow t wave, prominent u wave

hyperkalaemia- wide flat p wave, tall peaked t wave, widened qrs

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33
Q

describe RMP for hypo/hyperkalaemia

A

hypo- rmp increased, cell hyperpolarised
hyper- rmp decreased, depolarised cell

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34
Q

symptoms hypo hyperkalaemia

A

hypo- muscle weakness, tetany, vasoconstriction, thirst due to impaired ash, metabolic alkalosis due to increased intracellular H+

hyper- muscle weakness, cardiac arrhythmias

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35
Q

treatment hyperkalaemia

A

calcium gluconate to stabilise myocardium
insulin to lower plasma K+
calcium resonium to reduce K+ in body

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36
Q

describe transport of k+ across nephron

A

PCT- solvent drag
LoH- NKCC
DT/CD- ROMK

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37
Q

apical transporters in proximal tubule

A

Na+ glutamate/AA/organic transporter
Na+H+ antiport (amiloride)
Cl- Base antiport

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38
Q

apical transporters ascending loop of henle

A

NaKCC (Loop diuretic)
ROMK

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39
Q

apical transporters distal tubule

A

NaCl (thiazide)
ENaC
Ca2+ uniport

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40
Q

apical transporters principal cell collecting duct

A

Aquaporins
ENaC
ROMK out

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41
Q

apical transportes in alpha intercalated cell

A

H+ out
K+H+ antiporter (K+ in)

42
Q

apical transporters in beta intercalated cell

A

K+ out
Cl-HCO3- antiporter (Cl- in)

43
Q

effects of alkalaemia

A

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
Q

effects of academia

A

increases free ions by causing calcium ions to enter solution. causes arrythmias

45
Q

control of pH in PCT

A
46
Q

alpha intercated cell

A
47
Q

beta intercalated cell

A
48
Q

how to calculate anion gap and what causes it

A

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
Q

what causes metabolic alkalosis

A

excessive vomiting

50
Q

pre renal causes of AKI

A

hypovolaemia, shock (septic, hypovolaemia,cardiogenic), ischaemia (NSAIDS pre G ACE post G), cardiac shock

51
Q

renal causes of AKI

A

vasculitis

acute tubular nephritis- rhabdomyolytis and myoglobin causing ischemia

acute interstitial nephritis- nephrotoxic drugs

52
Q

nephrotic syndrome triad and treatment

A
  • oedema
  • hypoablumenia
  • protinurea >350ml/mmol

treat hypertension, diuretics, ACEi

53
Q

4 things causing nephrotic syndrome

A

diabetes, FSGS, membranous GN, minimal change GN

54
Q

triad of neprhitic syndrome and treatment

A
  • haematuria
  • hypertension
  • reduction in GFR

treat hypertension, manage CVS risk factors, steroids/immunosuppresants, oedema

55
Q

4 things causing nephritic syndrome

A

goodpastures

IgA nephropathy

rapidly progressive GN

post streptococcal GN

56
Q

how does CKD cause bone disease

A

reduced renal function

reduced Vit D resporption

reduced calcium

PTH released

bone resorption

57
Q

2 types periotneal dialysis

A

APD, CAPD

58
Q

treatment of CKD hyperkalaemia and acidosis

A
  • oral NaHCO3 tablets
  • reduce K+ intake, stop ACEi, avoid K+ increasing drugs
59
Q

how to measure extend of CKD

A

G1-G5 measurs GFR

A1-A3 measures albumin in urine

60
Q

which receptors mictruition

A

voiding (parasympathetic) M3

storage (sympathetic) B3, A1

61
Q

investigations incontenence

A

cytoscopy, urodynamics, frequency volume, pad test, urine dipstick

62
Q

medication incontenence

A

duloxetine- serotonin and NA inhibitor. increases IUS contraction

63
Q

surgery incontenence

A

intramural bulking, mesh

male sling, artficial sphincter

64
Q

describe development of urogenital sinus

A

the urorectal septum splits the cloaca into the urogenital sinus and anal canal

65
Q

describe the derivatives of urogenital sinus

A

upper- bladder

pelvic part- entire urethra in females, and the prostatic and membranous urethra in males.

phallic/caudal part- spongy urethra in males.

66
Q

what are the excretory and collecting sections of kidney formed from

A

excretory- intermediate mesoderm acted on by ureteric bud to form metanephric blastema.

collecting- ureteric bud

67
Q

3 things that make kidney

A

pronephros

mesonephros

metanephros

68
Q

formation of bladder in males

A
  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
Q

where do loop, thiazide and K+ sparing act and example of each

A

loop- LoH. inhibit NKCC. furesomide

thiazide- DCT. NaCl. bendroflumethiazide

K+- DCT, CD. block ENaC. amiloride/spironalactone

70
Q

which conditions treated by loop diuretics

A
  • Nephrotic syndrome
  • Renal failure
  • Cirrhosis of liver (spironolactone preferred)
  • hyperkalaemia
  • hypercalcaemia
71
Q

use thiazide diuretics

A

hypertension

72
Q

use aldosterone antagonists

A
  • Reduces mortality in heart failure
  • Preferred drug for cirrhosis (ascites & oedema)
  • Additional therapy in hypertension caused by primary hyperaldosteronism
73
Q

use ENaC blockers

A

Usually used in combination with K+ losing diuretics such as Loop or Thiazide diuretics to minimise K+loss

74
Q

use carbonic anhyrase inhibitors

A

glaucoma

75
Q

use osmotic diuresis

A

cerebral oedema

76
Q

what antibiotic sumple UTI

A

rimethoprim or nitrofurantoin (3 day course)

77
Q

treatment complicated UTI

A

Trimethoprim, nitrofurantoin or cephalexin (5-7 day course)

78
Q

treatment pyelonephritis

A
  • Co-amoxiclav (14 day course)
  • Ciprofloxacin (effective as a 7 day course)
  • Gentamicin (IV only – nephrotoxic)
79
Q

2 most common bacteria in females

A
  • e coli
  • staphyloccus saprophyticus
80
Q

RCC

  • what is it
  • risks
  • presentation
  • investigations
  • treatments
A
  • 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
Q

TCC

  • what is it
  • risks
  • presentation
  • investigations
  • treatments
A
  • 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
Q

TCC upper urinary tract

A
  • haematuria and obsturction
  • nephro-ureterectomy
83
Q

most common renal carcinoa

A

RCC

84
Q

risks polycystic kidney disease

A
  • causes steadily progressive CKD and can cause subarachnoid haemorrage
  • bleeding into cysts
85
Q

simple cortical cysts vs polycystic kidney disease

A

simpel cortical cysts dont reduce kidney function

86
Q

daily requirements

A

30ml/kg/day water
1mmol/kg/day Na+ K+ Cl-
50-100g day glucose

87
Q

water %

A

baby 75%

elderly 45%

woman 50%

88
Q

Mechanism osmotic duiresisp

A

Expands ECF volume initially, decreases blood viscosity, inhibit renin release, increase renal blood flow

89
Q

Use osmotic diuretics

A

Acute renal failure due to shock, acute drug poisoning, reduce intracranial pressure

90
Q

Side effects osmotic diuretics

A

Headache, nausea, vomiting (hyponatraemia). ECF expansion and so makes HF worse, dehydration and hypernatraemia

91
Q

formation of bladder females

A
  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
Q

what does the mesonephros form in adults

A

the trigone

93
Q

which pathogen

-ve nitrites

+ve leucocyte esterase

A

staphylococcus sapprophyticus

94
Q

which pathogen

+ve nitries

+ve leucocyte esterase

A

e coli

95
Q

treatment overactive bladder

A

antimuscarinic

96
Q

treatment SUI

A

duloxetone

97
Q

multiple myeloma signs

A

increased globulin, calcium, kidney size and recurrent infections

98
Q

findings SLE

A

wire loop thickening

99
Q

findings membranous glomerulonephritis

A

thickened capillary loop

100
Q

ions in sweat

A

anion- cholide

cation- sodium

101
Q

where do renal arteries originate

A

abdominal aorta, below SMA

ESA3 wrong answers (5 decks)

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