pathophysiology of renal stones by Sirajuddin Raeesah Firdhouse , 2nd year MBBS , Mahsa university

1. Akkshaya suresh kumar
BMS17091909
Year 2
Anatomy of the urinary tract

2. • Text
Anterior relations :
LR

3. ● Text
Posterior relations:
RL

4. ● Text
BLOOD SUPPLY TO THE KIDNEY

5. TEXT
CONSTRICTIONS
1. Ureteropelvic junction
2. Pelvic inlet
3. Uretrovesical junction
URETER :‣ 25 - 30 cm length and 3-4 mm in diameter
‣ descends on top of the psoas major muscles.

6. ● Text ‣ In the abdominal region ,apart from
the renal artery ,the branches from
gonadal artery ,the aorta ,and
common iliac artery anastomose
with each other .
‣ During operations , in the posterior
abdominal region , surgeons pay
special attention to the location of
the ureter and their blood supply
and are careful not to retract them
unnecessarily .
TO THE URETER,

7. ● Text‣ As they cross the pelvic brim , the
ureters are in very close proximity
to the ovaries.
‣ Approximately ,2cm above the
ischial spine , the ureters run
underneath the uterine artery .
‣ In male , instead of uterine artery
,the vas deferens cross the ureter
anteriorly .
CLINICAL IMPORTANCE :

8. Urinary bladder :
‣ Located anteriorly in the pelvic cavity , just posterior to the pubic bone .
‣ Trigone is a smooth triangular area between the opening of the ureter and the
urethra on the inside the bladder .

9. TEXT
RELATIONS :
AT THE BASE :
SUPERIOR SURFACE :
ANTERIOR SURFACE : ( Inferolateral )
‣ Retropubic space
‣ Puboprostatic ligaments
‣ Obuturator internus and Levator ani
APEX :
‣ Median umbilical ligament .
‣ Rectovesical pouch in the male
‣ Vesico uterine pouch in female
‣ Peritoneal cavity containing loops of ileum
‣ Sigmoid colon
‣ Uterine cervix

10. ● Text
TO THE BLADDER ,

11. • Text
Innervation
‣ T11 -L2 nerves
‣ Contraction of the internal sphincter
‣ Inhibitory to the detrusor muscle
SYMPATHETIC :
PARASYMPATHETIC :
‣ S2 -S4
‣ Pelvic splanchnic nerves , inf. Hypogastric nerve plexus .
‣ Motor of detrusor muscle ,inhibitory to the internal urethral sphincter in males .
SOMATIC AND PUDENDAL NERVES :
‣ S2- S4
‣ Innervates the external urethral sphincter (voluntary )

12. TEXT
SPHINCTERS IN URETHRA:
Sphincter vesicae :
‣ Surrounds the internal urethral orifice .
‣ Supplied by sympathetic fibres from T11— L2.
Sphincter urethrae :
‣ Surrounds the membranous part of the urethra .
‣ Supplied by pudendal nerve from S2, S3 and S4.

13. THANK YOU
REFERENCE :
• GRAY’S ANATOMY
• Clinical anatomy , Richard S. Snell , Edition 9
• https://www.earthslab.com/anatomy/kidneys/#content-location
• https://teachmeanatomy.info/abdomen/viscera/kidney/
• https://teachmeanatomy.info/pelvis/viscera/urethra/

14. Pathophysiology of renal stones
Sirajuddin Raeesah Firdhouse
BMS17091830
Year 2

15. Renal stones
 Renal stones are polycrystalline structures that form
from components of urine.
 The development of kidney stones is influenced by the
concentration of stone components in the urine , the
ability of the stone components to complex and form
stones , and the presence of substances that inhibit stone
formation.
 Stones require a nidus to form and a urinary environment
that supports continued crystallization of stone
components.

16. Aetiopathogenesis
• Increased blood or
urinary levels of
stone components
Interactions
among the
components
Anatomic changes
in urinary tract
structures
Metabolic and
endocrine
influences
Dietary and
intestinal
absorption factors
Urinary tract
infection

17. Types of renal stones
Calcium oxalate
monohydrate
Calcium
phosphate
Uric acid
Struvite stone Cysteine

18. Composition and contributing
factors to renal stones
Type of stone Contributing factors
Calcium ( oxalate and phosphate) Hypercalcemia and
hypercalciuria,
hyperparathyroidism, intestinal
bypass surgery.
Magnesium ammonium phosphate
(struvite)
Urea splitting urinary tract
infection
Uric acid ( urate ) Formed in acid urine with pH of
approx 5.5, gout , high purine
diet ,
Cystine Cystinuria ( inherited disorder of
amino acid metabolism )

19. Pathophysiology of real stone
formation
• Stasis of urine flow predisposes to
supersaturation of the urine with the particular
element that first become crystallized and then
become stones.
• Damage to the lining of the urinary tract.
• Decreased inhibitor substance in urine which
would otherwise prevent supersaturation and
crystalline aggregation.

20. Pathophysiology of renal stone formation

21. Pathogenesis of stone formation
Stone formation
Crystal growth and aggregation
Crystals inter-reaction
Crystallization, nucleation, growth and aggregation
Urinary supersaturation
Supersaturation depends on urinary pH, solute
concentration, ionic strength, and complexation. More the ions , more risk of stone formation
Stasis of urine flow
Predisposing factor for renal damage

22. Pathology
Mechanical obstruction of urine outflow results in :
 Increased backflow pressure into the kidneys
 Progressive hyperactivity and hypertrophy
 Progressive dilatation of renal calyces and pelvis
 Muscular loss of peristaltic activity leading to; stagnation of urine,
increased risk of infection , increased risk of formation of stones.
 Progressive atrophy of renal parenchyma
 Induce non-infective inflammation in interstitial tissue of the
kidneys.
 Compression of the arcuate artery leading to ischemic atrophy.
The effects depend on
either the obstruction is
unilateral or bilateral.

23. Microbiological aspect of renal
stones

24. Urolithogenic organisms.
•
Urea splitting
organisms:
• Proteus
providentia
• Staphylococcus
aureus
• Klebsiella
• Pseudomonas
• Mycoplasma
Urea splitting organisms
result in excessive
production of ammonia and
urinary alkalization leading
to the formation of
STRUVITE STONES (
magnesium ammonium
phosphate stones .

25. Urea splitting organisms
Proteus, Pseudomonas, Klebsiella,Mycoplasma

26. Urea splitting organisms

27. References.
• https://en.wikipedia.org/wiki/Struvite
• https://www.slideshare.net/reebababythomas/re
nal-calculi-ppt
• Harrisons principles of internal medicine
• Robbins and cotrans pathology
• Essentials of pathophysiology- Carol Matttson
Porth
•

28. Biochemistry of renal
calculi
Abdun Nafay
Year 2

29. Type to enter a caption.

30. 1. Calcium stones
•Consist of >90% oxalate with trace
amounts of phosphate.
•An estimated 40–60% of all calcium stone
formers have hypercalciuria.
•Occur primarily in individuals who excrete
excess levels of oxalate in urine.
•Primary hyperoxaluria, a rare autosomal
recessive condition, causes disturbances in
the oxalate biosynthetic pathway, leading to
very high oxalate excretion

31. Calcium oxalate stones

33. 3. Uric acid stones :
• Uric acid (UA) is an end product of
purine metabolism that the body
excretes in urine.
• Both purine overproduction and
excess purine ingestion favor
formation of UA stones.
• The three major risk factors for UA
stones are low urine pH (<5.5), low
urine volume, and hyperuricosuria.

35. Uric acid stones

36. 4. Struvite stones :
• Struvite stones consist of a mixture of
magnesium, ammonium, and phosphate
• Bacteria (Proteus, Staphylococcus,
Klebsiella, and Pseudomonas) hydrolyse
urea to produce NH4+ and OH– ions that
contribute to the alkalinity of urine.
• Both ammonium and alkaline urine are
essential for struvite supersaturation of
urine.

37. Struvite stones

38. 5. Cystine stones :
• Mutations in two genes, SLC3A1 and
SLC7A9 cystinuria
• Because cystine has limited solubility,
increased levels in urine favor its
precipitation and contribute to formation of
cystine stones
excrete increased amounts of
urinary cystine.

39. Cystine stones

40. References:
•https://www.aacc.org/publications/cln/arti
cles/2012/december/kidney-stones
•https://www.stonedisease.org/calcium-
oxalate-monohydrate-kidney-stone

41. Clinical manifestations
of urolithiasis
Hajira Shahid
Year 2

42. Clinical manifestations
● May be asymptomatic
● Severe renal colic and abdominal pain.
● Larger stones often manifest themselves by hematuria.
● Nausea/ vomiting
● Loin pain occurs - can be dull or sharp, constant or
intermittent.
● Complete anuria - suggestive of complete bilateral
obstruction.
● Polyuria (may occur in partial obstruction)
● Infection may lead to malaise, fever and septicemia.

43. Symptoms of bladder outflow obstruction
● Symptoms may be minimal.
● Diminished force of urinary stream, terminal
dribbling and sense of incomplete bladder
emptying.
● Infection commonly occurs causing-
a. Increased frequency
b. Urgency
c. Incontinence
d. Dysuria
e. Passage of cloudy, smelly urine.

44. Complications
● Serious infection of the kidney diminishes renal
function
● Urinary fistula formation
● Ureteral scarring and stenosis
● Ureteral perforation
● Urinary outflow obstruction : hydronephrosis -
chronic renal failure.

46. Workup

47. References
● Kumar and Clark Clinical Medicine 8th Edition
● Harrison Manual of Medicine 19th Edition
● Davidson’s Essentials of Clinical Medicine
● https://emedicine.medscape.com/article/437096-clinical
● https://www.mayoclinic.org/diseases-conditions/kidney-stones/symptoms-causes/syc-
20355755
Thank you