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urology final boss > Nephrolithiasis- epidemiology, types of stones, specific risk factors for stone formation, pathophysiology > Flashcards

Nephrolithiasis- epidemiology, types of stones, specific risk factors for stone formation, pathophysiology Flashcards

1
Q

intro of Nephrolithiasis

aka’s

locations in the UT

origin of formation

A

Synonyms

urolithiasis, kidney stones, renal calculus, urinary stones, stone disease.

Predilection in UT: may occur in all anatomical parts of urinary tract, they are formed in the kidney, except some bladder stones.

strictly speaking nephrolithiasis, refers to stones located in the kidney and in the ureter i.e located in upper urinary tract.

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2
Q

Epidemiology of nephrolithiasis

  • 3 reasons why it’s a disease in Evolution
  • scientific incidence in pop/ year.
    • what is a stone belt. when is crude rate used
  • age-> typical distribution
  • gender
A

evolution of nephrolithiasis is due to

  1. Epidemiological changes of the disease
  2. New diagnostic and therapeutic modalities e.g. minimally invasive surgical methods for treatment of stones •
  3. Availability of specific prophylaxis for population at risk for urinary stone disease

Incidence of Nephrolithiasis

  • it has a standardised incidence rate for scientific purpose of 7/100000 pop/yr —> this is a moderate incidence rate
  • Stone belt= areas of the world w/ higher rates of imdt to high
  • Crude rate used locally

ages affected by Nephrolithiasis

  • Typical bimodal distribution
    • 20-50 & 60-80
  • Peak incidence= 30-50
    • ​this makes nephrolithiasis a socially improtant disease

Gender DIstribution of Nephrolithiasis M:F = 4:1

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3
Q

ages affected by Nephrolithiasis

A

Typical bimodal distribution

20-50 & 60-80

Peak incidence= 30-50

​this makes nephrolithiasis a socially improtant disease

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4
Q

standardised incidence of Nephrolithiasis rate per year for scientific purpose

A

of 7/100000 pop/yr

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5
Q

list the 8 Stone location in urinary tract in Nephrolithiasis

rarest location

type of stone located in renal pelvis and calyces

3 locations of stones in ureter

2 possible locations of stones in the distal ureter

why is bilateral kidney stones unfabourable and what is the %

A
  1. Very rarely they are located in the renal parenchyma - nephrocalcinosis In upper - middle - lower calyces
  2. In renal pelvis
  3. Renal pelvis + calyces —> stag horn calculus
  4. Pelvic ureteric junction area
  5. Upper ureter
  6. Middle ureter •
  7. Distal ureter —> juxtavesical and intramural
  8. Ureteric orifice

15-20% bilateral kidney stones which is unfavourable as is a special form of uro or nephrolithiasis

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6
Q

Stone=Chemical composition of renal stones

  • list all 6 types with the following formula
    • composition and alternative names,
    • percentage if relevant
    • cause
    • presence or abscence in the normal urine sediment
    • ph level - if relevant
    • gross
    • x ray appearance
    • most common
  • dx betw/ composition and classification
A
  1. Calcium nephrolithiasis —> 75%.
    • types
      • ​​calcium oxalate monohydrate (Vevelite)
      • calcium oxalate dihydrate (Vedelite)
      • calcium phosphate (Apatite)
    • 75%.
    • xray: radioopaque, _dense_ -> rough surface causes colic
  2. Uric acid nephrolithiasis—> 10%
    • ​d/2 Gout/ Polycythemia which leads to elevated urate excretion —> “hyperuricosuria”
    • Formed in acidic pH of urine
    • x ray: radioluscent**= pure uric. usually assoc w/ ca stone
  3. Cystine stones
    • d/2: congenital defect in metabolism of 4 amino acids: COAgL= -Cystine -Ornithine -Arginine -Lysine
    • Cystine is NOT a normal component of urine sediment
    • presence of cystine in urine - cysteineuria
    • x ray: radioluscent
  4. Xanthineuria
    • d/2: congenital gene defect of enzyme xanthine dihydrogenase,
      • catalyses hypoxanthine to xanthine and xanthine to urea
    • xanthine is ALSO NOT a normal component of urine sediment - Xanthinuria
      • Formed in acidic pH of urea
    • x ray: radioluscent
  5. Magesium ammonium phosphate
    • aka struvite/ stag horn stone in renal prelvis & calyx
    • formed during in UTI , which changes ph urine to alkaline
    • alkaline pH caused by UTI both of which make struvite grow faster
    • assyx
    • xray: poor radioopaque. mx
  6. drug induced nephrolithiasis
    • most common is xanthine nephrolithiasis,
    • caused by patients with HPV/HIV, using antiviral drugs
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7
Q

describe calcium stones

A

Calcium nephrolithiasis —> 75%.

types

  1. ​​calcium oxalate monohydrate (Vevelite)
  2. calcium oxalate dihydrate (Vedelite)
  3. calcium phosphate (Apatite)

75%.

xray: radioopaque, dense -> rough surface causes colic

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8
Q

describe Uric acid nephrolithiasis

A

Uric acid nephrolithiasis—> 10%

​d/2 Gout/ Polycythemia which leads to elevated urate excretion —> “hyperuricosuria”

Formed in acidic pH of urine

x ray: radioluscent= pure uric. usually assoc w/ ca stone

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9
Q

describe Cystine stones

A

Cystine stones

d/2: congenital defect in metabolism of 4 amino acids: COAL= -Cystine -Ornithine -Arginine -Lysine

Cystine is NOT a normal component of urine sediment

presence of cystine in urine - cysteineuria

x ray: radioluscent

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10
Q

describe Xanthineuria stones

A

d/2: congenital gene defect of enzyme xanthine dihydrogenase,

catalyses hypoxanthine to xanthine and xanthine to urea

xanthine is ALSO NOT a normal component of urine sediment

Formed in acidic pH of urea

x ray: radioluscent

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11
Q

describe Magnesium ammonium phosphate stones

A

aka struvite/ stag horn stone in renal prelvis & calyx

formed during in UTI , which changes ph urine to alkaline

formed in alkaline pH caused by UTI both of which make struvite grow faster otherwise have weak growth

assyx

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12
Q

describe

drug induced nephrolithiasis

A

most common is xanthine nephrolithiasis,

caused by patients with HPV/HIV, using antiviral drugs

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13
Q

classification of stones

NB: different from composition

composition: what it’s made of
classifcation: physical properties=

number, gross appearance, location

A
  • 1)stone size : measures diameter
  • Up to 5 mm in diameter —> simple renal stones
  • 5-10 mm; —> simple renal stones
  • 10-20 mm —> simple renal stones
  • 20+ mm in largest diameter or in the kidney with anomaly —> complex renal stones

2)Stone location —> NB! defines clinical presentation of the disease

  • Nephrocalcinosis: in renal parenchyma
  • Staghorn calculus: in renal pelvis & calyces
  • Ureter: Upper, Middle, Distal :Juxtavesicalar and intramural
  • Urinary bladder

3)gross- size, colour, number

  • ca- Sharp, brown with blood (s)
  • MgAmPh- Largest filling the calyxes
  • uric - hard, red-brown (mx)
  • cyst- hexagonal &Yellow (mx)
  • xanthine - smooth round red (

X ray characteristics —> on plain radiography —> plain kindey ureter bladder radiography subdivided into:

  • radiopaque (+) —> calcium oxalate stones, vivelite,videlite,apatite
  • poor radiopaque (+/-) —> struvite
  • radioluscent (-) —> uric acid stones, cystein and xanthine stones
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14
Q

what is the main indication for the use of x ray radiography for renal stones

(KUB)

A

to find radioopaque/ poor radioopaue stones

luscent stones are not indicated

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15
Q

why is the composition of the stone important

A

it affects the treatment used e.g.

calcoum oxalate has hard composition and requires Extracorporeal lithotripsy

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16
Q

what is the causal genesis of nephrolithiasis

list the 3 types of causative factors & give examples for each

percentage of people with familiy history

A

1)Exogenous factors:

such as climate (hot and dry) and lifestyle (no physical activity) •

2)Endogenous factors

  • such as heredity and family predisposition 1/4 — 25% in patients have a family history of nephrolithiasis
  • race —> Armenians and Arabs- white men particularly affected
  • diseases that increase risk for stone formation

3)Local factors important from surgical ​pov

  • Mechanical/ congenital anomalies:
    • 1)Horseshoe, 2)PUJ, 3)Stenosis, 4)Uretocele
  • Dynamic: Pregnancy-> hormones cause atony of UB. rxed with stent
17
Q

what is the current trend for nephrolithiasis

A

Trend in nowadays for nephrolithiasis -n Incidence for nephrolithiasis is increasing

18
Q

list some diseases that increase the risk of neprolithiasis by increasing the risk of stone formation

stone says GBE stone MI kuro

A
  1. Genetic defects; Cystnuria, -> cystein/xanthine stones
  2. Bone diseases: Osteoporosis, -> calcium stones
  3. Endocrine diseases:
    • Hyperparathyroidism —> hypercalcaemia and hypercalciuria
  4. Metabolic diseases: Gout or podagra- uric acid stone
  5. Intestinal diseases lead to hyperoxaluria and primary Oxaluria e.g.
    1. Crohn’s disease
    2. intestinal resection(bariatric surgery)
19
Q

what is uretocelle

20
Q

what is horseshoe kidney

21
Q

what is PUJ

A

Congenital obstruction at the renal pelvis.

rare in adults, UPJ obstruction may happen after kidney stones, surgery or upper urinary tract swelling.

blockage slows or stops the flow of urine out of the kidney.

causes urine to pool in the kidney, which leads to kidney swelling (hydronephrosis). Often, only 1 kidney is affected. The enlarged kidney is easily seen on prenatal ultrasound.

sx =

abdominal mass, UTI with fever , flank pain (pain in the upper abdomen or back, mostly with fluid intake), kidney stones, bloody urine, poor growth in infants

dg

lab- RFT- BUN, Creatinine

imaging intravenous pyelogram (IVP) / nuclear renal scan

CT in acute case

rx

1) Open Surgery- pyeloplasty - UPJ is removed, and the ureter is reattached to the renal pelvis to create a wide opening
2) Laparscopic pyeloplasty - w/w/o robot
3) Internal Incision w/ wire

22
Q

Pathogenesis —> formal genesis of renal stones

what are the four factors of stone formation (EESS)

A
  1. Elevated levels of lithogenic substances in urine
    • ​urine is hypersaturated but stable until one sub ↑
      • ​hyperuricosuria (↑urates in urine)
      • hyperoxaluria,hyperphosphauria
      • hypercalciuria(↑ oxalate in urine)
      • cysteinuria- cong defect of amino acid met
      • xanthinuria cong defect of hypoxanthine by xanthine dehyd->xanthint->uric acid
  2. Elevated levels of activators (nucleators) in urine
    • provoke heterogenous crystallisation in the urine e.g.
      • lithogenic subs
      • cells
      • sulphonamides like biseptol
  3. Shortage of inhibitors in urine
    • _​_form soluble chemical compounds with lithogenic substances.
    • their abscence promotes crystallization e.g.
      • 1)magnesium, 2)pyrophosphate, trace metals
  4. Suitable pH of urine
    • ​​4,5-5,0= acidic →urate stones
    • 6.0-6.5 = neutral →oxalate
    • > 7.0 — alkaline →struvite / phospate
23
Q

which are the Elevated levels of lithogenic substances in urine
​

A
  • urine is hypersaturated but stable until one sub ↑
  • ​hyperuricosuria (↑urates in urine)
  • hyperoxaluria,hyperphosphauria
  • hypercalciuria(↑ oxalate in urine)
  • cysteinuria- cong defect of amino acid met
  • xanthinuria cong defect of hypoxanthine by xanthine dehyd->xanthint->uric acid
24
Q

Elevated levels of activators (nucleators) in urine
provoke heterogenous crystallisation in the urine e.g.

A
  • lithogenic subs
  • cells
  • sulphonamides like biseptol
25
Q

Shortage of inhibitors in urine

​form soluble chemical compounds with lithogenic substances.

their abscence promotes crystallization

give the three examples

A

1)magnesium, 2)pyrophosphate, trace metals

26
Q

list the Ph’s for dx types of stones

A
  • ​​4,5-5,0= acidic →urate stones
  • 6.0-6.5 = neutral →oxalate
  • > 7.0 — alkaline →struvite / phospate
27
Q

list the 4 Mechanisms for the theory of crystallization

A
  1. Crystal embryo,
  2. Crystal growth,
  3. Crytsal aggregation,
  4. Manifestation — presence of stone in urinary tract
28
Q

Secondary pathological effects of the renal stones

moimu!

um moi?

A
  • Migration
    • migrating stones cause renal colic
    • Stationary stones such as stag horn calculus dont cause renal colic
  • Obstruction
    • obstruction of calyx — hydrocalicosis
    • obstruction of ureter —> hydronephrosis
    • Calculus anuria
  • Infection
    • recurrent UTI
  • Ulceration
    • leads to hematuria & renal and perirenal abscess
  • ​Malignisation
    • transitional epithelium of upper urinary tract may transform into squamous epithelium - metaplasia squamous cell carcinoma
29
Q

Classification of UROPATHIES aka urologial obstructions with examples?

urology final boss (22 decks)

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