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MS2 Renal > 9/18- Obstruction, Infection, and Stones > Flashcards

9/18- Obstruction, Infection, and Stones Flashcards

1
Q

What are some signs/symptoms associated with obstruction?

A
  • Decreased urine output
  • Flank pain
  • Renal colic/hematuria if associated with stone
  • Hesitancy
  • Dribbling
  • Frequency, nocturia
  • Recurrent UTIs (esp in men); PVR>50mL associated with 3-fold increase
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2
Q

What are some anatomical features of hydronephrosis (grossly)?

A
  • Very thin renal cortex with damaged glomeruli
  • Blunted pyramids
  • Dilated renal pelvic
  • Dilated calices
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3
Q

What are some anatomical features of hydronephrosis (ultrasound)?

A
  • Dilation of renal pelvis and calyces In pic, left is normal
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4
Q

What is this ultrasound showing?

A

Mega-ureter

  • Hydronephrosis?
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5
Q

What is this CT scan showing?

A

Left: kidney very large; swollen

Right: normal

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6
Q

When might you have obstruction with no dilation?

A
  • Hypovolemia
  • Retroperitoneal fibrosis
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7
Q

What may cause neurogenic bladder?

A
  • Stroke/TBI/Alzheimer’s
  • Spinal cord injury, MS, GBS, myelitis
  • Autonomic neuropathies/DM
  • Post-natal (spinal block) and narcotics
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8
Q

What can cause physiologic hydronephrosis?

A
  • Pregnancy: usually on right side
  • Renal allograft
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9
Q

What can cause urinary tract obstruction (common)?

A

Kids: most are congenital

Adults are BPH or stones

  • Women, think mass/malignancy unless proven otherwise!
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10
Q

What is a risk of urinary tract obstruction?

A

Urinary stasis -> infections that can spread to renal parenchyma (pyelonephritis) and urosepsis

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11
Q

T/F: anuria is essential to the diagnosis of obstruction?

A

False

  • Partial bostruction can -> polyuria, tubular damage (salt wasting) and fluid debt may result from accumulated fluid
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12
Q

What is the triophasic pattern of UTO?

A

Triphasic pattern of renal blood flow and ureteral pressure changes

1. GFR declines; RBF increases

  • GFR = Kf(Pgc - Pt - pi gc) because of Pt and collecting system pressure
  • RBF increases to counterbalance Pt in attempt to prserve GFR (NO, PGE)

2. P elevated but RBF begins decline next 3-4 hrs (Ang II, TXA2, Endothelin)

3. Further decline in RBF, then decrease in Pt and collecting system pressure also occurs (stabilizes) 5 hrs after obstruction

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13
Q

What are the early and chronic pathologic findings of UTO?

A
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14
Q

T/F: Caliectasis can persist for weeks after decompression of acute obstruction

A

True; caliectasis can persist for weeks as renal function improves

  • CKD (thinning cortex)
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15
Q

How can you treat kidney stones?

A
  • Hydration
  • Ureteral dilators (e.g. Flomax)
  • Urologic intervention
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16
Q

How can you treat RCC or bladder tumor?

A

Percutaneous stents

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17
Q

How can you treat urethral obstruction?

A
  • Catheterization
  • Cystostomy
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18
Q

What is the prognosis in pts with UTO?

A
  • Complete recovery usually occurs after 1 wk of obstruction
  • Minimal recovery occurs after 6 wks of obstruction
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19
Q

What are the long term consequences of UTO?

A
  • If obstruction >12hr, changes in collecting duct function can be dilated/hemorrhage zones; these alterations result in decreased responsiveness to ADH (can mimic nephrogenic DI)
  • Renal tubular acidosis; inability for kidneys to acidify urine, because hydrogen transporters are damaged
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20
Q

What is nephrolithiasis?

A

Kidney stones

  • Common
  • Easy to evaluate
  • Treatable
  • Preventable
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21
Q

Are kidney stones more common in men or women? Other epidemiology?

A

Men (12%, 6% women)

  • White > black
  • Very common in Middle Easterners
  • Bimodal in women (peaks at 35 and 55 yrs)
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22
Q

What is the most common kidney stone composition?

A

Calcium oxalate

23
Q

What are characteristics of Ca phosphate stones?

A
  • Radiopaque
  • Associated with hypercalciuria (50% will end up idiopathic)
24
Q

List stone composition possibilities

A
  • Calcium oxalate (no. 1)
  • Calcium phosphate
  • Struvite
  • Uric acid
25
Q

What are struvite stones?

A

Aka infection stones

  • Bacteria liberate large amts of ammonia from urine urea, raising pH and combining with Mg/P to form mineral (struvite)
  • Alkaline pH
  • Urinary debris and crystal niduses

Stones composed of: Mg, Ca, ammonium, phosphate, carbonate (struvite)

  • Radiopaque!
  • Difficult or impossible to eliminate stones: staghorn calculi (cast of pelvicocalyceal system)
26
Q

What are uric acid stones?

A
  • 2-5% of stones
  • Potentiates calcium stone formation
  • Uric acid has 2 dissociable protons…
  • Consider high cell turnover (e.g. leukemia, myeloproliferative d/o)
  • Remember: urate stones are radiotranslucent!
27
Q

What causes cystinuria?

A

Autosomal recessive disorder

  • Cystine, ornithine, arginine, lysine not reabsorbed in urine
  • Cystine transport may be defective in gut and/or nephron

Cystine is a poorly soluble AA

Suspicion:

  • Young age
  • Family history
  • Hexagonal crystals
28
Q

What can cause drug stones?

A
  • Acyclovir
  • HAART (e.g. indinavir, atazanavir)
29
Q

What cause the Melamine milk crisis?

A
  • Infant milk supplemented with Melamine to raise protein content
  • 6 deaths
30
Q

What conditions favor stone formation?

A
  • Slow urine flow
  • High solute concentration

Results in supersaturation of the urine with solutes that tend to crystallize and later form stones

31
Q

What is nucleation? How does it occur?

A

Appearance of solid-phase nucleus in a region that had previously had no solid phase

  • Hydroxyapatite formation involving renal papillae; Randal’s plaques; serve as nidus for crystallization/extension for Ca containing stones
  • Typically starts in basement membrane of thin limbs; in thin LH, slow flow, hyperosmotic mucopolysaccharide matrix, electrostatically charged ionic sites -> ripe template to begin crystallization
32
Q

What can predispose someone to stones (broadly)?

A

Decreased inhibitor substances in the urine that would otherwise prevent supersaturation and crystalline aggregation

33
Q

What are some inhibitors of urinary crystallization?

A
  • Multivalent metallic cations (Mg)
  • Small organic (citrate)
  • Inorganic anions (Pyrophosphate)
  • Macromolecules ranging in size from 10kd
  • 100 kd (e.g. Tamm-Horsfall protein) Citrate and Mg are the most significant inhibitors
  • Citrate is the most important physiologic inhibitor (shown to increase Ca solubility and coat crystals and prevent growth and aggregation)
34
Q

What can cause idiopathic hypercalciuria?

A
  • Absorptive: excessive Ca absorbed from GIT
  • Renal leak: impaired tubular Ca reabsorption
  • Renal phosphaturia: renal Pi losses which causes increased GI reabsorption of Ca and hypercalciuria
35
Q

What can cause secondary hypercalciuria?

A

Elevated serum Ca

  • Sarcoidosis, TB, other granulomatous diseases
  • Malignancy (Lymphoma, bone mets, myeloma, others)
  • Paget’s disease of bone
  • Immobilization

Endocrine

  • Hyper PTH, hyperthyroid, Cushing’s syndrome

Medications

  • Loop diuretics, Vit D supp

Renal tubular acidosis

Medullary sponge kidney

36
Q

Does calcium oxalate inhibit or promote stone formation?

A

Oxalate potentiates Ca stone formation

37
Q

What can contribute to high levels of Ca oxalate?

A
  • GI absorption increased with low Ca and Mg diets ( Low GI calcium increases oxalate absorption)
  • Malabsorption syndromes (e.g., bacterial overgrowth, short bowel, pancreatitis, IBD, surgical procedure, blind loop syndromes, celiac dz …etc).

—- Increased fatty acid in intestine -> Ca–salts-fatty acids -> Ca not available to bind oxalate -> increased Ox absorption.

  • Disordered Ox metabolism: pyridoxine (Vit B6) deficiency, primary hyperoxaluria
38
Q

How do hypo-citraturia and magnesuria affect stone formation?

A
  • Ca-citrate is more soluble than other Ca compounds, thus Ca available for crystallization is decreased

—- Use K-citrate to increase urinary citrate

—- K increases urinary citrate

  • Mg binds oxalate in soluble compound, removing it from crystallizing with Ca
39
Q

How does bariatric surgery affect stone formaton?

A

(Roux-en-Y gastric bypass (RYGB) or small-pouch Gastric bypass)

  • Risk for stones/renal failure (oxalate nephropathy) equal to that of a patient with primary oxaluria

(Gastric banding not associated with risk of nephrolithiasis)

40
Q

What is the ultimate factor for stone formation?

A

Concentration of the solute

  • Therefore, reduced urine volume will amplify the saturation of all solutes and raise risk of stone
41
Q

What to suspect in history of someone with stones?

A
  • History previous stones, frequent urinary infection, hyperparathyroidism, sarcoidosis, RTA, malignancy
  • Strenuous exercise during summer
  • Medication and diet histories
  • Family history of stone disease
  • Chronic Foley, stent, other instrumentation
42
Q

Different presentations of kidney stones?

A
  • Attached to papilla: hematuria but not significant pain
  • Lodged stones; sever flank/back pain with radiation into groin
  • Nausea, vomiting, urinary frequency, gross hematuria
43
Q

Common places kidney stones may lodge?

A
  • Ureteropelvic junction (10.6%)
  • Proximal ureter (23.4%)
  • Where ureter crosses anterior iliac vessels (1.1%)
  • Distal ureter (4.3%)
  • Ureverovesical junction (60.6%)
44
Q

What is important in the acute evaluation of kidney stones?

A
  • Hx = most important
  • Serum: basic metabolic profile

Urine:

  • UA (hematuria), culture and sensitivity
  • DO NOT perform urinary profile during acute stone work-up (not representative)
  • Stone analysis if one available
45
Q

T/F: You may not see a stone that is already in the ureter on renal ultrasound?

A

True

46
Q

What is the imaging method of choice for kidney stones?

A

CT scan- images kidney and ureter

47
Q

Pros and cons of IVP?

A
  • Widely available
  • Shows urinary tract very well
  • Disadvantage: requires IV contrast
48
Q

How to treat acute stone?

A
  • Confirm diagnosis, R/O renal failure and sepsis
  • Pain relief; IVF; +/-alpha blocker; +/- ureteroscopy/ureteral stent
  • Follow-up to confirm stone passed
  • Decide on level of evaluation

—- If first stone, no other disease or family history, screen patient with routine lab

—- If multiple stones, family history, or renal failure, more detailed workup

49
Q

What is ESWL?

A

Estracorporeal shock wave lithotripsy (ESWL)

  • Noninvasive
  • Effective for stones under 1 cm, especially distal ureteral stones or lower pole stones
50
Q

What is URS?

A

Ureteroscopy

  • Invasive
  • Effective for all stones including > 1 cm
51
Q

What are the odds of recurrence of kidney stones without preventative therapy?

A
  • 20%: 1-3 yrs
  • 40-50% by 5 yrs
  • 50-60% by 10 yrs
  • 75% by 20-30 yrs
52
Q

What are methods to prevent stones?

A
  • Drink 3L/d to ensure at least 2 L urine/d (don’t guide therapy by urine color)
  • Juice does NOT reduce risk (grapefruit juice increased risk)
  • Limit salt intake under 3 g/d (increased urinary elimination of salt -> more Ca in urinary filtrate; low Na increases proximal Na reabsorption which increases renal tubular Ca reabsorption)
  • Limit intake of nuts if due to hyperoxaluria
  • Hypokalemia decreases urinary citrate
  • Higher K intake has been inversely associated with new stone formation in men/older but not younger women
  • Decrease animal protein (associated with new stone formation in men but not women)
  • Less vitamin C (supplement increases urine oxalate)
  • More Mg: complexes with oxalate (decreasing in urine) and may decrease oxalate absorption in gut
53
Q

What is some pharmacologic intervention for stones?

A
  • Thiazides: decreases urinary Ca
  • Allopurinol for hyperuricosuria
  • Pyridoxine for primary hyperoxalauria
  • Potassium Citrate for hypocitrituria/ acidotic states or low urine pH
  • Abx therapy for urea-splitting organisms
  • Cystine-binding drugs increase solubility 50-200x: D-penicillamine, 2-mercaptopropionylglycine, captopril
  • ?Probiotic: O. formigenes (gut flora) is associated with 70% reduction in risk for recurrent stones
54
Q

Concepts to remember:

  • Obstructive nephropathy frequent and causes can vary widely (have suspicion)
  • Triphasic patter of UTO
  • Early relief of obstruction results in improved prognosis
  • Remember stone types and crystal appearance
  • Strong genetic component (cysteine, Ca stones, but also diet/co-morbidity (e.g., uric acid)
  • Acute management
  • Chronic prevention (stone prevention)
A

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MS2 Renal (25 decks)

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