Obstructive Kidney Disorders Flashcards
Diabetus mellitus is associated with Acute or Chronic Renal Insufficency
Chronic (think pathophysilogy)
What type of cancer my migrate to urinary system and/or peritoneum and cause Bi-lateral hydronephrosis in females?
CERVICAL
Why creatinine incr in blood in post-renal faliure, like in urethral obstruction?
Incr hydrostatic pressure in Bowmans space, DECR GFR–>less filtration.
What role plays Citrate in kidney stones formation?
-Prevent aggregation of urine crystals.
Most common stones are:
Ca++-oxalate> Stuviate> uric acid> cysteine.
Risk Factor for Ca++-oxalate stone formantion? (5)
-Hypercalcemia–.Sarcoidosis and HyperPTH
-Hypercalciuria-Hypocalcemia (give Thiazide)
-Hypocitrauria
-Fat malasbp.
-Anti-Freeze (ethylene glycol)
-Vit C. overdose
Diagnosis
Radio-opaque on both X-ray and CT scan with ENVELOPED shape crystal?
Ca++-oxalate ot Ca++-phosphate stones
Diagnosis
Patient is tachypnic because he went for high mountain trip for 2 weeks and he recieves medication and comes with flank pain that “hurts a lot”
Ca++-Phosphate stone–>Acetozolamide (alkalanization of urine)
Whats the risk factor for Ca++-Phosphate stone?
Alkalanization of urine.
Treatment of Ca++ stones?
-Thiazide, Hydrate, Low NaCl diet, K+ Citrate,prevent oxalate rich foods (tomatos,oranges,spinach)
Whats the benefit of not eating oranges in Ca++-oxalate stones?
-Reducing consumption of oxalate.
Struviate stones is made up off…
Ammonium, Phosphate, and Magnesium..
What organism is associated with struviate stones?
-Urease + organisms
What stones is only treated with surgery 100% of the time?
-Staghorn calculi or Struviate stones–> to large to be expelled in urine.
What stones is only treated with surgery 100% of the time?
-Staghorn calculi or Struviate stones–> to large to be expelled in urine.
COLA ???
-a.a that are falied to be reabsp in PCT in Cysteine stones.
-Cysteine, orithine, lysine, arginine
Hexagonal, yellow shape stones?
-Cysteine stones.
Diagnosis
Staghorn calculi with NO history of UTI..
-Cysteine stones.
Stones that prefer to grow in pH>4.5
-Ca++ and struviate
Stones that prefer to grow at pH<3.5
-Treatment
cystine and uric acid stones
-K+ Bicarbonate
Diagnosis test for Cysteine stone?
-Na+ Cyanide-Nitropurraside Test (detects Cysteine in urine).
Associations for uric-acid stones?
-Leukemia (high cell turnover) and Gout
-Chemotherapy
Rhomboid shaped crystals?
-Uric acid stones
Diagnosis
We identify a stones but on imaging is negative?
-Uric acid stones
Treatment for uric acid stones?(2)
K+ Bicarbonate
and
Allopurinol (Xanthine Oxidase inhb.–>reduces uric acid production)
A-Ca++ stone
B- Coffin stone (struviate)
C-Staghorn
D-Rhomboid (uric acid)
E-Hexagonal (Cysteine)
Unilateral flank side pain//Colicky pain that radiates ipsilateral groin +vomiting +nausea+ described as a pain like “labor”
-Side sympt:Hematuria,WBC cast…..
-On palpabation tender.
-Kideny stone//Nephrolitaisis
What treatment can be done for every Kideny stones?
-Hydration.
What test should always be done in patients with kidneys stones?
**Urine analysis.. **
Commonest presentation of kidney stones..
-Hot day, playing outside without drinking to much water–>flank pain..–>imaging suggest stone.
-Palpation they are tender.
3 most commonest areas that stones lodge?
-pelvic prim (ureters pass common iliac vessels)
-ureter-pelvic junction (supperiorly)
-vesiculo-uretic junction (ureter enters bladder)
Why Kideny stones cause unilateral pain mostly?
-They lodge above bladder affecting ine side USUALLY
How is chemotherapy relate uric acid stone?
-Chemotherapy can lead to** tumor lysis syndrome,** ncreased uric acid release into the urine, increasing the risk of uric acid stone formation.
-Prevention and treatment include aggressive hydration,allopurinol,rasburicase.
Cysteine stones presentation?
-Family history of stones formation + hexagonal stone.
Diagnosis
-due to increased oxalate levels secondary to malabsorption.
Fat malabsp. (Ca++-oxalate stone)
What type of epithelium lines bladder
-Transithional epi (umbrela epi)
How does urination work?
-Strech recep in bladder–>as bladder fills it will send signals to S2-24 (Micturition refelex)–>1.Send signals to Pontine center in brain–>controls external sphinter (drain it to overide the micturition refelx)
2.Micturition reflex will INCR. Prasympathtic (detrusar activation and sphinter relaxation) + **DECR Sympathetic stimuli **(decr internal sphinter tone)
-All is left in hands of Pontine center to urinate.
Causes of neurogenic bladder..
-Syphylis, HSV, Diabetic nueropathy, Spinal cord injuries,Multiple Sclerosis***
-Spinal cord lesion above T12 causes what type of bladder lesion?
-Complication?
-Spastic Bladder
-Loss of communication between Pontine center and Micturition reflex–>Bladder contracts but NO control over sphinter–>cannot urinate
-Incr pressure of bladder–>Backflow–>Hydronephrosis.
Bladder dosent contract lesion?
-Flaccid lesion (LMN lesion)–>Urinary retention
-Acute optic neuritis,weakness,spasticity,neurogenic bladder, paraparesis, MRI isgold standard Periventricular plaques
-Common FEMALE 20-30’s
Multiple Sclerosis ass **Spatic Bladder due to de-mylination.
-We give Muscarinic antagonist to relax detrussor muscle.
What are the 2 most common congenital obstructions renal system?
-Post urethral valve and vesicu-uretere reflux
Vesico-ureter reflux pathophysiology?
-The ureter is shorter enetring the bladder–>when bladder gets full–>you have backflow to kidneys.
Posterior urethral valve pathophysiology..
-Complications
-Imaging
-Most common obstruction in MALE infants.
-Overgrowth of bladder into prostatic urethra–>incr pressure and backlow.
-Ass with BI-LATERAL Hydronephrosis and recurrent UTI’s
-Imaging: thick bladder and dilated prostaic urethra.
Compliaction of congenital instruction is…
Potter sequence.
Potter sequence causes(3)
-Complications
-Congenital urinary obstructions (2),Bilateral renal agenesis, uteroplacental Insufficency—>oligohydramnios–>Potter sequence.
-Pulmunary Hypoplasia///wrinkle skin.wide separated ears, flattened faces.
When does fetus strat producing urine?
-20 week (weel developed urinary system)
Presentation of: uteropelvic obstr., placental insufficency, urethral obstruction.
-Ureteropelvic junction obstruction typically manifests with unilateral hydronephrosis.
-Placental insufficiency can lead to decreased blood flow to the fetus and subsequently decreased urine production or amniotic fluid, but NO kidney enlargement**
-urethral obstr–>BILATERAL Hydronephrosis and oligohydramnios
Pathophysiology of Horseshoe kideny..
-Associated with..
-When both kidneys fuse in pelvic area–>at week 8 when move up will cause impingement at Inf Mesenteric artery–>dosent move all the way up-> incr risk of ureter obstruction–>hydronephrosis or Potter sequence.
-Turners syndrome and Trisomies (13,18 and 21)
Uteric bud forms….
Blastema forms…
-ureter,calyces,collecting ducts and tubules
-kidney
Reasson of agenesis
-Uteric Bud dosent influenze your blastema.
-Uni-lateral agenesis
-Bi-Lateral agenesis
-NO oligohydramnios, hyperthrophy of one kidney–>hypertension and renal faliure
Potter sequence
What causes Hydronephrosis?
-Kidney stones, Congenital anatomical defects, cervical cancer, Neurogenic bladder,pregnancy,BPH
Pathogenesis of Hydronephrosis?
-Compression atrophy–>atrophy of cortex and medulla.
Diagnosis and which one is worst prognosis
Hydronephrosis and letf side is worst–> extends all the way to renal paranchyma.
-Infants—congenital defect of pleuro peritoneal membrane left-sided herniation (right hemidiaphragm is relatively protected by liver)
-Diaphragmatic hernia–>pulmunary hypertension.
