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Urinary > S7 - renal stones > Flashcards

S7 - renal stones Flashcards

1
Q

what is urolithiasis?

A

the formation of stones in the urinary tract

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2
Q

where can renal stones form? most common site?

A

anywhere in the urinary tract

most common in renal pelvis

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3
Q

how do renal stones form?

A

single or multiple
80% unilateral
often recurrent, especially if an untreated predisposing factor is present

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4
Q

how can renal stones form within the urinary tract?

A

minute (like sand)
staghorn calculi (cast of pelvic & calyceal system
large concretions in bladder

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5
Q

locations where urinary stones form?

A 
urinary calyx
urinary pelvis 
staghorn (filing pelvis)
mid-ureteral stone
bladder stones
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6
Q

why have urinary stones incidence decreased?

A

better diet & living conditions

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7
Q

when are urinary stone formations seen?

A

in low protein diet, chronic diarrhoea & dehydration
increased oxalate consumption
vitamins A, B1, B6 deficiencies
magnesium deficiency

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8
Q

what is lithotomy?

A

surgical removal of a calculus from bladder, kidney or urinary tract

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9
Q

what are complications of lithotomy?

A

haemorrhage, infection, fistulae, incontinence

erectile dysfunction

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10
Q

what are causes of bladder stones?

A

bladder outflow obstruction
presence of foreign body
passed down form upper urinary tract

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11
Q

what are examples of bladder outflow obstruction?

A

urethral stricture
neuropathic blader
prostate obstruction

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12
Q

what are examples of presence of foreign body?

A

catheter

non-absorbable sutures

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13
Q

what can bladder stones lead to?

A

anuria (<100ml/day)

painful bladder distension

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14
Q

what are renal stones?

A

solid material formed in kidneys from minerals in urine

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15
Q

what are renal stones also called?

A

kidney stone
renal calculus
nephrolith

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16
Q

when is the usual onset of renal stones?

A

usually after 30 years
ratio of men:women = 2:1 (except struvite stones more common in women)
affects 1-5% UK population

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17
Q

what are renal stones made of?

A

calcium stones (99%)

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18
Q

what are the types of calcium stones?

A

calcium oxalate combine with calcium phosphate (forming apatite) - 65% (mix of both)
calcium phosphate alone (15%)

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19
Q

when is calcium phosphate alone stones seen?

A

in hyperparathyroidism & renal tubular acidosis
(metabolic acidosis enhances renal calcium excretion through its effect on TRPV5 in the distal tubule. Besides increased efflux of calcium, the simultaneous release of bicarbonate from bone buffers the metabolic acidosis: B-IC)

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20
Q

when else is calcium stones seen?

A 
uric acid (3-5%) - less Ca2+
apical H+/K+ antiporter doesn't work, more proton retention &amp; K+ excretion
so calcium phosphate stones form in lower pH
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21
Q

what other calcium stones are there?

A

struvite (infection stones) - more common in women (UTI)
urease stones - (breakdown urea to ammonia & CO2)
triple phosphate stones (magnesium ammonium phosphate hexahydrate - from infection by bacteria which have urease)
10-15%

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22
Q

aside from calcium, what other types of renal stones are there?

A
  1. cysteine stones (in rare genetic disorder e.g. cystinuria)
  2. drug stones e.g. indinavir (HIV), triamterene (diuretic), sulphadiazine (antibiotic)
  3. ammonium acid urate stones
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23
Q

why do urinary stones form?

A

if there is urine supersaturation with minerals

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24
Q

when do you get urine supersaturation with minerals?

A
  1. solvent contains more solute than it can hold in solution
  2. seed crystal forms by nucleation - first step in formation of a new structure via self assembly
  3. physical, not chemical reaction
    e. g. mentos & coke (mentos has more layers of sugar than coke can hold)
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25
Q

how can urine become supersaturated with minerals?

A
  1. decrease in water content
  2. increase in mineral content
  3. decrease in solubility of solute in urine (change in urinary pH)
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26
Q

when can you get a decrease in water content?

A

dehydration

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27
Q

when do you get an increase in mineral content?

A
  1. hypercalcaemia (calcium in blood) & hypercalciuria (calcium in urine) - calcium oxalate stones
  2. hyperoxaluria (excess oxalate in urine)
  3. hyperuricaemia (uric acid in blood) & hyperuricosuria
  4. cysteinuria (cysteine in urine)
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28
Q

when do you get a decrease in solubility of solute in urine?

A
  1. some solutes more soluble at high pH and some at low pH

2. renal tubular acidosis results in persistently alkaline urine (B-ICells) & decrease urinary citrate excretion

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29
Q

which stone does acidic urine favour the formation of?

A

calcium oxalate & uric acid stones

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30
Q

which stone does alkaline urine favour the formation of?

A

calcium phosphate stones

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31
Q

when does calcium phosphate precipitate and what is it dissolved by?

A

precipitates in alkaline medium
dissolved by acid (chicken bones in vinegar)

as calcium phosphate is main calcium in bones

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32
Q

which stone is supersaturation likely to form?

A

uric acid & cysteine stones

calcium based stone formation may be more complex

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33
Q

how do renal stones form?

A

majority (75%) calcium oxalate stones appear to grow like stalactites attached to exposed interstitial deposits of calcium phosphate
‘Randall’s plaque’ on the tips of renal papillae (subepithelial calcification of the renal papilla)

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34
Q

how can renal stones form aside from calcium oxalate on Randall’s plaque?

A

otherwise stones can form on plugs protruding from ducts of Bellini or free in solution (ducts of Bellini drain into renal papillae)

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35
Q

what are calcium oxalate stones that grow on the tips of renal papillae (Randall’s plaque) composed of?

A

composed of core of calcium phosphate surrounded by calcium oxalate

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36
Q

what are other causative factors of renal stones formation?

A
  1. urine stasis
  2. drugs
  3. genetic / congenital factors
  4. no apparent abnormalities / cause
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37
Q

how do you get urine stasis?

A
  1. low urine flow
  2. obstructive
  3. infection
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38
Q

what are genetic / congenital factors that cause renal stones?

A
  1. primary metabolic disturbances e.g. cystinuria (high concentrations of the amino acid cystine in the urine, form cystine stones)
  2. kidney abnormalities e.g. polycystic kidneys, medullary sponge kidneys
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39
Q

what are calcium oxalate stones associated with?

A

5% associated with hypercalcaemia & hypercalciuria
55% have hypercalciuria (urine) withuot hypercalcaemia
5% associated with hyperoxaluria (oxalate in urine)

40
Q

when do you get hypercalcaemia & hypercalciuria? (5%) in calcium oxalate stones

A

e.g. in hyperparathyroidism, diffuse bone disease, sarcoidosis (granulomas develop in organs of body)

41
Q

when do you have hypercalciuria (urine) without hypercalcaemia? (55%) in calcium oxalate stones

A

can be associated with hyperabsorption of calcium from gut
OR
impairment in renal tubular absorption of calcium (calcium just floods out into urine)

42
Q

when do you get calcium oxalate stones associated with hyperoxaluria? (5%)

A

hereditary / secondary to intestinal OVERabsorption (of oxalate) in patients with ENTERIC diseases e.g. Crohn’s disease

43
Q

how is calcium stored in body? why?

A

calcium is very potent ion, must be well regulated
calcium homeostasis - precarious balance
more than 99% body calcium locked away in skeleton

44
Q

what pumps calcium out of cells?

A

cell membrane
concentration of calcium in cytoplasm LOW IN CELL
(1.5mM outside of side, 1x 10-7M in cells)
Ca2+ ATPase / NXC (3Na+:Ca2+)

45
Q

what is concentration of calcium regulated by?

A

effects of PTH
1,25-dihydroxycholecalciferol (calcitriol,1,25-dihydroxyvitamine D) - increase blood Ca2+
calcitonin (C cells of thyroid - lowers blood Ca2+, opposite of PTH)

all act on gut, kidney & bone

46
Q

where are calcium sensing receptors?

A

present in parathyroid glands, kidney, brain & other organs

47
Q

describe calcium homeostasis of PTH

A

increases serum calcium:
increase osteoclast resorption of bone (rapid)
increase intestinal absorption of Ca2+ (slow)
increase synthesis of calcitriol (1,24-(OH)2D3
increase renal tubular reabsorption of calcium
increase excretion of phosphate (don’t form apatite - increase free serum Ca2+

48
Q

how does vitamin D play a role in calcium homeostasis?

A

increase calcium absorption in gut
increase calcification & resorption in bone
(both increase Ca2+ in body)
no role in kidneys

49
Q

describe calcium homeostasis in terms of calcitonin

A

produced by thyroid C cells
decreases serum calcium by:
1. inhibiting osteoclastic bone resorption
2. increasing renal excretion of calcium & phosphate

50
Q

what is the most common metabolic abnormality in calcium stone formers?

A

hypercalciuria (55%)

51
Q

what are the causes of hypercalciuria?

A
  1. idiopathic
  2. hypercalcaemia
  3. excessive dietary intake of calcium
  4. excessive resorption of calcium from skeleton
52
Q

when do you get excessive resorption of calcium form skeleton leading to hypercalciuria?

A 
prolonged immobilisation (bed/wheelchair bound)
weightlessness (astronauts)
53
Q

when do you get idiopathic causes leading to hypercalciuria?

A

in most patients that have increased absorption of calcium from GIT

54
Q

what do you use to reduce the risk of renal stone formation? (in spaceflight - weightlessness)

A

potassium citrate

55
Q

what are causes of hypercalcaemia?

A
  1. hypersecretion of PTH resulting in increased bone resorption
  2. destruction of bone tissue
  3. other mechanisms
56
Q

what are the most common causes of hypercalcaemia?

A

primary hyperparathyroidism & malignancies (release PTHrP)

57
Q

when do you get hypersecretion of PTH resulting in increased bone resorption leading to hypercalcaemia?

A
  1. primary: parathyroid hyperplasia / functional tumour
  2. secondary: to renal failure (which causes retention of phosphate - therefore hypocalcaemia - apatite)
  3. ectopic: secretion of PTHrP by malignant tumour (e.g. squamous cell carcinoma of lung - non-small cell)
58
Q

when do you get destruction of bone tissue leading to hypercalcaemia?

A
  1. primary tumour of bone marrow e.g. myeloma
  2. diffuse skeletal metastases
  3. paget’s disease of bone (accelerated bone turnover)
  4. immobilisation (reduced bone formation whilst bone resorption continues)
59
Q

what are the causes of hypercalcaemia via other mechanisms?

A
  1. excessive vitamin D ingestion
  2. thiazide diuretics (block NCC)
  3. sarcoidosis (macrophages activate a vit D precursor)
  4. milk-alkali syndrome (excessive calcium intake)
60
Q

what are the main clinical signs of hypercalcaemia?

A

severe muscle weakness (less likely to depolarise - hyperpolarise - opposite of hypocalcaemia = tetany)

painful bones - fractures
renal stones
abdominal graons (constipation, peptic ulcers, pancreatitis, gallstones)
psychic moans (depression, lethargy, seizures)

61
Q

what is hyperoxaluria?

A

rare autosomal recessive genetic disorders of oxalate synthesis (primary hyperoxaluria types 1 & 2)

62
Q

what does hyperoxaluria cause?

A

increased intestinal oxalate absorption secondary to GI disease (e.g. Crohn’s disease) usually with an intestinal resection (increased absorption of oxalate from colon)

63
Q

what dietary habits can lead to hyperoxaluria?

A

high oxalate intake (spinach, rhubarb, tea, nuts)

low calcium intake (increases GI absorption of oxalate)

64
Q

what are struvite stones?

A

UTIs & urinary stones

struvite stones are mixed infective stones

65
Q

what are struvite stones composed of?

A

magnesium ammonium phosphate with variable amounts of calcium

66
Q

how do you normally get struvite stones?

A

usually secondary to infection with organisms (e.g. Proteus mirabilis) with the enzyme urease which hydrolyses urea to ammonium hydroxide

also, production of mucoprotein from infection provides an organic matrix on which stones can form

67
Q

what do struvite stones normally lead to?

A

formation of a large cast of the collecting system - staghorn calculus

68
Q

when can urinary stones (struvite) be seen in people predisposed to UTIs?

A

spinal cord injury
neurogenic bladder
vesicoureteric reflux (backflow form bladder to kidney)
obstructive uropathy (backup of urine because can’t drain through ureter)

69
Q

when are uric acid stones seen?

A

in hyperuricaemia
also in people with tendency to have urine with pH < 5.5
radiolucent (can’t be seen on x-ray)

70
Q

when is uric acid produced?

A

end point of purine metabolism

71
Q

when do you get hyperuricaemia?

A
  1. in idiopathic gout

2. secondary consequence of increased cell turnover

72
Q

when do you get secondary consequence of increased cell turnover leading to hyperuricaemia?

A
  1. lympho or myeloproliferative disorders
  2. after chemotherapy (tumour lysis syndrome)
    (1. 8% pts after lymph / myeloproliferative disorder develop renal stones after chemotherapy)
73
Q

when do you get dehydration?

A
  1. in presence of acidic urine

2. patients with ileostomies - dehydration & loss of bicarbonate from GI secretions

74
Q

how do renal stones present?

A 
most asymptomatic - seen on radiograph
renal colic
stones in kidney - dull ache in loins 
recurrent UTIs
haematuria
renal failure
urinary tract obstruction (fluid intake increased, results in increased pain)
75
Q

describe renal colic

A

excruciating pain

lasts about 20-60mins

76
Q

what causes renal colic

A

by peristaltic contractions / spasms of ureter as it attempts to expel the stone

77
Q

where can renal colic pain radiate from to?

A 
from flank (side) to iliac fossa &amp; testes / labium OR inner thigh
(distribution of 1st lumbar nerve root)
(embryological link between urinary tract, GIT &amp; gonads - urogenital sinus (bladder &amp; ureter) separated from GIT by urorectal septum - intermediate mesoderm)
78
Q

what is renal colic pain often accompanied by?

A

nausea & vomiting

pallor, sweating & restlessness

79
Q

what is common in renal colic pain? when does it subside?

A

haematuria

untreated, subsides in a few hours

80
Q

what are the investigations in urolithiasis?

A
  1. MSU (mid-stream urine)
  2. serum
  3. plain abdominal x-ray
  4. CT kidney, ureter & bladder
  5. can pass urine through a sieve & catch calculi for chemical analysis
81
Q

what do you test for in mid-stream urine in investigating urolithiasis?

A

RBCs
urinary casts (mould of tubules containing RBC & WBC)
urinary crystals
culture - cause / consequence of stones?

82
Q

what is urolithiasis?

A

formation of stony concretions in bladder or urinary tract

83
Q

what do you test for in serum in investigating urolithiasis?

A

U&E
creatinine
calcium levels

84
Q

when do you use plain abdo x-ray?

A

60% stones are radiopaque (calcium-containing stones especially)
uric acid stones are radiolucent (CAN’T see on x-ray)

85
Q

what would you use CT kidney, ureter & bladder to investigate urolithiasis?

A

better than USS - almost ALL stones can be seen
ideally during pain
can see stones & dilated renal pelvis
can see uric acid stones (radiolucent)
identifies any primary renal disease predisposing to stone formation

86
Q

what size urinary stone can be passed?

A

sizes varies between sand like to large stones
<5mm diameter can be passed (90%)
>7mm diameter usually require urological intervention

87
Q

what complications can occur with urinary stones?

A
  1. acute pyelonephritis (inflammation of kidney tissue, calyces, renal pelvis) +/- gram negative septicaemia
  2. pressure necrosis (stress/strain leading to tissue damage) of the renal parenchyma
  3. urinary obstruction and hydronephrosis (kidney stretched / swollen - urine buildup)
  4. ulceration through the wall of the collecting system
88
Q

how can we treat urinary stones?

A
  1. analgesia (IV diclofenac / pethidine)
  2. warmth to site of pain
  3. bed rest

ureteroscopy
percutaneous nephrolithotomy
extracorporeal shock wave lithotripsy (ESWL)

89
Q

when do we use ureteroscopy?

A

to look for stones in bladder / lower ureter

90
Q

what is percutaneous nephrolithotomy?

A

put a little incision (usually for stones in renal pelvis) through skin and go into the kidney and open up pelvic calyces & fish out the stone then stitch up

91
Q

when is extracorporeal shock wave lithotripsy (ESWL) used?

A

most commonly for stones near renal pelvis

92
Q

what does extracorporeal shock wave lithotripsy (ESWL) do?

A

lithotriptor delivers external, focused, high intensity pulses of ultrasonic energy (blast the stone)
takes 30-60mins
fragments stones - to be passed spontaneously

93
Q

how do you prevent stones from forming in the first place?

A

decrease urine supersaturation

94
Q

how do you decrease urine supersaturation to prevent stones from forming in the first place?

A
  1. drink more water (all stones type)
  2. decrease excretion of calcium / oxalate
  3. potassium citrate alkalinise urine
95
Q

how do you decrease excretion of calcium / oxalate?

A

thiazide diuretic (cause reabsorption of Ca2+ from urine)

96
Q

how does potassium citrate alkalinise urine prevent stones forming?

A
  1. reduce risk of calcium oxalate, uric acid & cysteine stones
  2. forms soluble complexes with calcium ions
  3. can induce calcium phosphate stones

Urinary (13 decks)

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