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Pediatrics BRS > Chapter 11 - Renal > Flashcards

Chapter 11 - Renal Flashcards

1
Q

How are an individual’s maintenance fluid requirements calculated?

A
  • 100 mL/kg/d for the first 10 kg of body weight
  • 50 mL/kg/d for the second 10 kg of body weight
  • 20 mL/kg/d for each additional kilogram
  • more if they have excess insensible losses as in respiratory distress or if febrile
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2
Q

What is the maintenance sodium and potassium requirement?

A
  • sodium is 2-3 mEq/kg/d

- potassium is 1-2 mEq/kg/d

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3
Q

In what two ways do we classify dehydration?

A
  • based on severity or degree

- and based on serum sodium concentration as hypo-, iso-, or hypernatremic

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4
Q

Rehydration of a hemodynamically unstable patient always begins with what?

A

a 20 mL/kg bolus of isotonic saline or LRs

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5
Q

Over what time period do we typically correct dehydration? Why?

A
  • over 24 hours for hyponatremic or isonatremic dehydration to prevent central pontine myelinolysis
  • over 48 hours for hypernatremic dehydration to prevent cerebral edema
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6
Q

What is the reasoning behind oral rehydration therapy?

A
  • it is a combination of glucose and electrolytes
  • intestinal absorption of sodium and other electrolytes is enhanced by the active absorption of glucose through co-transport
  • this cotransport process continues to function normally even in cases of secretory diarrhea while other sodium absorption pathways are impaired
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7
Q

For which patients is oral rehydration therapy insufficient?

A
  • those with severe dehydration
  • those with paralytic ileum or GI obstruction
  • those with extremely rapid stool losses or repeated severe emesis losses
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8
Q

How do we define microscopic hematuria?

A

as 6 or more RBCs per high-power field, detected on three or more consecutive samples

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9
Q

Why is hematuria defined as 6 or more RBCs per high-power field, detected on three or more consecutive samples?

A

because, like proteinuria, many children have transient microscopic hematuria and a single positive test is not considered evidence of pathology

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10
Q

RBC casts are indicative of what?

A

glomerulonephritis

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11
Q

How does RBC morphology alter the interpretation of microscopic hematuria?

A
  • if the RBCs originated in the glomerulus, they are usually dysmorphic with blebs in the RBC membrane
  • those that appear normal more likely originated form the lower urinary tract
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12
Q

What does it mean if a patient has a urinary dipstick positive for blood but no RBCs are found on microscopic urinary analysis?

A

since dipsticks pick up hemoglobin and myoglobin, it is suggestive of hemoglobinuria or myoglobinuria without hematuria

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13
Q

How do we test for proteinuria?

A
  • a 24 hour urinary protein collection is most accurate but difficult
  • instead, we use a random spot uric total protein-to-creatinine ratio
  • TP/CR should be less than 0.5 if 6-24 months old and less than 0.2 if older
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14
Q

What is a normal TP/CR?

A

less than 0.5 if the individual is 6-24 months old and less than 0.2 if they are older

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15
Q

What is benign transient proteinuria?

A

transiently increased urinary protein excretion associated with vigorous exercise, fever, dehydration, and congestive heart failure in children

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16
Q

What is orthostatic proteinuria?

A
  • a benign condition in which there is an increase in urinary protein excretion while upright but not supine
  • diagnosed based on an elevated afternoon TP/CR but normal first-morning urine TP/CR
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17
Q

What is the difference between glomerular proteinuria and tubular proteinuria?

A
  • glomerular is caused by an increase in permeability of the glomerular capillaries to large molecular weight proteins
  • tubular proteinuria is decreased reabsorption of low molecular weight proteins, especially B2-microglobulin, by tubular epithelial cells
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18
Q

What does finding B2-microglobulin in the urine suggest?

A

it is a low molecular weight protein that filters but is usually entirely reabsorbed through the tubular epithelium; because of this, finding it in the urine is indicative of tubular proteinuria and suggests a pathology such as interstitial nephritis, ischemic renal injury, or tubular injury form a nephrotoxic drug

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19
Q

What is a nephritic syndrome?

A

characterized by glomerular damage due immune complex deposition, activation of complement, C5a-mediated neutrophil chemotraction

  • proteinuria is limited (< 3.5 g/day)
  • oliguria and azotemia
  • salt retention with periorbital edema and hypertension
  • hematuria and RBC casts
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20
Q

What are the signs and symptoms of nephrotic syndrome?

A
  • a syndrome of hypoalbuminemia, hypogammaglobulinemia, a hyper coagulable state, and hyperlipidemia/hypercholesterolemia due to glomerular dysfunction
  • protein loss contributes to pitting edema, loss of Ig increases the risk of infection, antithrombin III loss increases coagulability, and lipids may result in fatty casts in urine
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21
Q

Poststreptococcal Glomerulonephritis

A
  • also known as acute proliferative glomerulonephritis
  • presents with it is a nephritic syndrome of hematuria, proteinuria, hypertension, and edema 2-3 weeks after a group A, beta-hemolytic strep infection
  • diagnosis is based on clinical features, low serum complement, and detection of a prior strep infection with ASO or ADB titers
  • renal biopsy is only indicated if the patient has significant renal impairment or nephritic syndrome
  • glomeruli appear hyper cellular on light microscopy and granular, subepithelial deposits of IgG, IgM, and C3 are identified on EM
  • treatment is supportive as children rarely progress to renal failure; this means fluid restriction, antihypertensive meds, and protein, sodium, potassium, and phosphorus restriction
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22
Q

IgA Nephropathy

A
  • the most common nephropathy worldwide
  • it is due to IgA complex deposition in the mesangium
  • presents during childhood with episodic hematuria with RBC casts present in urine, typically following mucosal infections
  • diagnosed via renal biopsy which shows mesangial proliferation and increased mesangial matrix on light microscopy
  • treatment is supportive
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23
Q

Membranoproliferative Glomerulonephritis

A
  • presents as a nephritic syndrome or as a nephrotic syndrome with hematuria as well as low serum complement
  • type I is characterized by subendothelial deposits and an associated with HBV and HCV
  • type II is characterized by intramembranous, “ribbon-like” deposits and C3 nephrotic factor (an antibody that stabilizes C3 convertase; see low levels of C3 in patient)
  • light microscopy reveals a “tram-track” appearance
  • IF reveals granular immune complex deposition
  • there is no definitive treatment and most patients develop end-stage renal disease
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24
Q

Describe the pathogenesis that leads to hypercholesterolemia as a part of nephrotic syndrome.

A
  • reduced plasma oncotic pressure induces increased hepatic production of plasma proteins, including lipoproteins
  • at the same time, plasma lipid clearance is reduced because of reduced activity of lipoprotein lipase in adipose tissue
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25
Q

Most mortality associated with nephrotic syndrome is caused by what?

A
  • thrombosis following the loss of antithrombin III

- S. pneumoniae infection following the loss of immunoglobulins

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26
Q

Describe four steps that should be taken in the management of nephrotic syndrome.

A
  • IV infusion of 25% albumin
  • implementation of a salt restriction
  • corticosteroids for MCD; use cyclophosphamide or cyclosporine for steroid-resistant patients
  • blood culture to evaluate for pneumococcal infection if the child is febrile
27
Q

Minimal Change Disease

A
  • the most common cause of nephrotic syndrome in children
  • usually idiopathic, but may be associated with Hodgkin lymphoma
  • glomeruli appear normal on light and electron microscopy, but effacement of foot processes can be seen on EM
  • proteinuria is selective (only albumin)
  • respond extremely well to steroids, suggesting damage is mediated by cytokines
28
Q

Hemolytic Uremic Syndrome

A
  • endothelial damage due to drugs or infection (primarily shiga toxin-producing bacteria like E. Coli, O157:H7), which results in the pathologic formation of platelet microthrombi, consuming platelets and shearing RBCs
  • often presents with a diarrheal prodrome, if shiga toxin-mediated, followed by sudden onset hemolytic anemia, thrombocytopenia with mucocutaneous bleeding, and acute renal failure
  • other findings include increased bleeding time, normal PT/PTT, elevated LDH, decreased haptoglobulin, and schistocytes present on blood smear
  • treat with plasmapheresis and corticosteroids; transfusions as necessary; manage renal failure
  • antibiotics are contraindicated in cases driven by shiga-like toxin
29
Q

Alport’s Syndrome

A
  • an X-linked dominant type IV collagen defect
  • results in thinning and splitting of the glomerular basement membrane, leading to progressive nephritis
  • presents with hematuria, hypertension, sensory hearing loss, and ocular disturbances
  • treated with ACE inhibitors to slow renal disease, management of hypertension, and eventually renal transplant
30
Q

Medullary Cystic Kidney Disease

A
  • an autosomal dominant defect leading to cysts in the medullary collecting ducts
  • fibrosis of the parenchyma results in shrunken kidneys (as opposed to the enlarged, cystic kidneys of PKD)
31
Q

Autosomal Recessive PKD

A
  • an inherited defect leading to bilaterally enlarged kidneys with cysts in the renal cortex and medulla
  • presents in infants as worsening renal failure with hypertension and possibly Potter sequence
  • associated with congenital hepatic fibrosis, leading to portal hypertension and hepatic cysts
  • requires transplantation
32
Q

Autosomal Dominant PKD

A
  • an inherited defect leading to bilaterally enlarged kidneys with cysts in the renal cortex and medulla
  • due to an APKD1 or APKD2 mutation
  • presents in young adults as abdominal pain, flank masses, hypertension, hematuria, and worsening renal failure with cysts developing over time
  • associated with berry aneurysm, hepatic cysts, and mitral valve prolapse
33
Q

What defines significant, severe, malignant, and essential hypertension?

A
  • significant: greater than the 95th percentile
  • severe: greater than the 99th percentile
  • malignant: with evidence of end-organ damage
  • essential: without a clear etiology
34
Q

How should blood pressure be measured in infants and children?

A
  • infants should be measured while supine

- children and adolescents should be seated

35
Q

What are the two most common causes of hypertension in children 1-10 and in adolescents 10-18?

A
  • children: renal diseases and coarctation of the aorta

- adolescents: renal diseases and essential hypertension

36
Q

Renal Tubular Acidosis

A
  • an inability of the kidney to maintain normal acid-base balance, either congenital or acquired
  • symptoms vary based on the type of RTA but growth failure, vomiting, recurrent calculi, muscle weakness, bone pain, myalgia, and nephrocalcinosis are common
  • presents as a hypercholremic, non-anion gap, metabolic acidosis
37
Q

Type I Renal Tubular Acidosis

A
  • an inability of the kidney to maintain normal acid-base balance
  • due to an inability of the distal renal tubular alpha-intercalated cells to excrete acid
  • secondary to amphotericin B toxicity, analgesic nephropathy, congenital anomalies of the urinary tract, or SLE
  • presents with vomiting, growth failure, acidosis, and nephrocalcinosis
  • labs find urine pH > 5.5 and serum potassium low
  • treated with small doses of oral alkali
38
Q

Type II Renal Tubular Acidosis

A
  • an inability of the kidney to maintain normal acid-base balance
  • due to impaired bicarbonate reabsorption by the proximal renal tubular cells
  • secondary to fanconi syndrome, multiple myeloma, heavy metal ingestion, or carbonic anhydrase inhibitors
  • presents with vomiting, growth failure, acidosis, and muscle weakness
  • labs find urine pH < 5.5 as the kidneys try to compensate, and serum potassium is low
  • treated with large doses of oral alkali
39
Q

Type III Renal Tubular Acidosis

A
  • an inability of the kidney to maintain normal acid-base balance
  • it is a variant of type I due to an inability of the distal renal tubular alpha-intercalated cells to excrete acid but also complicated by proximal tubular bicarbonate wasting during infancy
  • due to an inability of the distal renal tubular alpha-intercalated cells to excrete acid
  • presents with vomiting, growth failure, acidosis, and nephrocalcinosis
  • labs find urine pH > 5.5 and serum potassium low
  • treated with large doses of oral alkali
40
Q

Type IV Renal Tubular Acidosis

A
  • an inability of the kidney to maintain normal acid-base balance
  • presents as a transient acidosis in infants and children with hyperkalemia as the hallmark
  • secondary to obstructive uropathy or aldosterone deficiency
  • may be asymptomatic or present with failure to thrive
  • labs find urine pH < 5.5 as the kidneys try to compensate, and serum potassium is high
  • treated with furosemide to lower serum potassium as well as with oral alkali
41
Q

How do we define oliguria?

A

as a urine output less than 1 mL/kg/hr

42
Q

How should renal failure be managed?

A
  • intravascular volume should be restored first and then total fluid intake should be restricted to the patient’s insensible losses plus output only
  • protein intake should be restricted
  • patients should be monitored with daily weights, frequent BP measurements, calculation of Is and Os, and monitoring of electrolytes
  • dialysis may be necessary if conservative management fails
43
Q

What happens to BUN/Cr, FENa, and urine osmolality in someone with pre-renal azotemia?

A
  • when RBF decreases, BUN reabsorption is enhanced and the BUN/Cr increases > 15
  • since tubular function is intact, FENa is normal (<1%) and urine osmolarity is normal (>500 mOsm/kg)
44
Q

What happens to BUN/Cr, FENa, and urine osmolality in someone with post-renal azotemia?

A
  • in the early stage, increased tubular pressure enhances BUN reabsorption, and the BUN/Cr increases > 15
  • in the early stage, tubular function is also normal with FENa < 1% and urine osmolarity > 500mOsm/kg
  • with long-standing obstruction, tubular damage ensues and the BUN/Cr falls, FENa rises, and there is an inability to concentrate urine
45
Q

Prerenal Acute Renal Failure

A
  • caused by a reversible decrease in renal perfusion that leads to a reduction in GFR
  • may be secondary to dehydration, hemorrhage, congestive heart failure, shock, or hypoproteinemic states
  • BUN/Cr ratio increases, urine specific gravity increases, urine osmolarity increases, and FENa is normal
46
Q

Intrarenal Acute Renal Failure

A
  • may be due to damage to the glomerulus as in PSGN, lupus nephritis, or HUS; in these cases, it presents with hematuria and proteinuria
  • may be due to damaged to the tubules (aka acute tubular necrosis) following ischemic injury with an increase in urinary B2-microglobulin and FENa above 1%
  • may be due to damage to the interstitium (aka acute interstitial nephritis) following exposure to various drugs and presenting with eosinophilia, eosinophilia, and an increase in urinary B2-microglobulin
47
Q

Acute Tubular Necrosis

A
  • the most common cause of acute renal failure
  • due to ischemia or nephrotoxicity in the form of aminoglycosides, heavy metals, myoglobinuria as in crush injury, ethylene glycol, radio contrast dye, or urate from tumor lysis syndrome
  • injury results in necrosis of tubular epithelial cells, which form brown, granular casts and diminish GFR
  • tubular dysfunction leads to elevated BUN and Cr, though the BUN/Cr is < 15, FENa > 1%, and Osm < 500
  • clinical features include oliguria as well as hyperkalemia and acidosis due to the inability to secrete these cations
  • reversible but requires supportive dialysis since electrolyte imbalances can be fatal
  • recovery takes 2-3 weeks as tubular cells are stable and take time to re-enter the cell cycle
48
Q

Acute Interstitial Nephritis

A
  • an intra-renal azotemia (acute renal failure)
  • characterized as a drug-induced hypersensitivity affecting the interstitium and tubules
  • most commonly due to the 5 P’s: Pee (diuretics), Pain-free (NSAIDS), Penicillins, Proton pump inhibitors, and rifamPin
  • presents with oliguria, fever, and rash lasting days to weeks
  • uniquely, eosinophils may be seen in urine
  • biopsy will reveal an inflammatory infiltrate in the interstitium
  • may progress to renal papillary necrosis
49
Q

Postrenal Acute Renal Failure

A
  • due to an obstruction of urine flow from either the kidney(s) or urethra
  • secondary to stones, tumors, ureterocele, urethral trauma, neurogenic bladder, or posterior ureteral valves in males
  • presents with dilation of the renal collecting system visible on ultrasound
  • in the early stage, increased tubular pressure enhances BUN reabsorption, and the BUN/Cr increases > 15
  • in the early stage, tubular function is also normal with FENa < 1% and urine osmolarity > 500mOsm/kg
  • with long-standing obstruction, tubular damage ensues and the BUN/Cr falls, FENa rises, and there is an inability to concentrate urine
50
Q

How do we manage end-stage renal disease?

A
  • nutritional management with avoidance of high phosphorus, high sodium, or high potassium foods
  • administration of oral phosphate binders and vitamin D analogs to prevent renal osteodystrophy
  • protein restriction
  • blood pressure monitoring and management
  • anemia treated with iron and EPO
  • growth hormone if growth fails to normalize
  • dialysis once GFR is less than 5-10% of normal
  • transplant once available
51
Q

What is prune belly syndrome?

A

a syndrome of absent rectus muscles, bladder outlet obstruction, and cryptorchidism

52
Q

Renal Agenesis

A
  • unilateral or bilateral absent kidney formation secondary to failure of the mesonephric duct or metanephric blastema to develop
  • unilateral leads to hypertrophy of the existing kidney and increases risk of renal failure later in life
  • bilateral leads to Potter sequence
53
Q

Dysplastic Kidney

A
  • a non-inherited, congenital malformation of renal parenchyma with cysts and abnormal tissue
  • may develop from any congenital obstruction and is more common than renal agenesis
  • usually unilateral, but the bilateral form must be distinguished from inherited polycystic kidney disease
  • bilateral leads to pulmonary hypoplasia and in either case, there is an association with concentrating defects, renal tubular acidosis, and varying degrees of renal insufficiency
  • a multicycstic dysplastic kidney is the most common cause of abdominal mass discovered in newborns
54
Q

What is the most common abdominal mass discovered in newborns?

A

multicystic dysplastic kidney

55
Q

Horseshoe Kidney

A
  • a most common congenital renal anomaly, in which the kidneys are conjoined, usually at the inferior pole
  • ascent of the kidneys is stopped by the inferior mesenteric artery, and they end up located in the lower abdomen
56
Q

Duplex Collecting System

A
  • a congenital renal anomaly in which the ureteric bud bifurcates before interacting with the metanephric blastema, creating a bifid ureter
  • can also arise if two ureteric buds interact with the same metanephric blastema
  • strongly associated with vesicoureteral reflux and ureteral obstruction, increasing the risk of UTI
57
Q

Vesicoureteral Reflux

A
  • caused by abnormalities of the ureterovesical junction, most often a short submucosal tunnel in which the ureter inserts through the bladder wall
  • has autosomal dominant inheritance
  • low grades typically resolve spontaneously while more severe forms may predispose to pyelonephritis and eventual reflux nephropathy with end-stage renal disease and hypertension
  • diagnosed with voiding cystourethrogram
  • treated with low-dose prophylactic antibiotics and surgical reimplantation of the ureters if severe
58
Q

Nephrolithiasis

A
  • a precipitation of a urinary solute as a stone
  • presents with colicky pain, hematuria, and unilateral flank tenderness
  • high concentration of solute and low urine volume are risk factors
  • usually passed within hours but may require surgical intervention
  • typically calcium oxalate, calcium phosphate, ammonium magnesium phosphate, uric acid, or cystine in nature
  • rare in children and providers should look for a predisposing metabolic disorder
  • risk factors include hypercalciuria, hyperoxaluria secondary to enteric malabsorption, distal RTA, hyperuricosuria, cystinuria, UTI and P. mirabilis in particular, or hyperparathyroidism
59
Q

Calcium Oxalate/Calcium Phosphate Nephrolithiasis

A
  • the most common type of kidney stone
  • the urine crystals have an envelope shape
  • usually due to idiopathic hypercalciuria or hyperoxaluria, which can be inherited or secondary to enteric malabsorption
  • treatment is HCTZ, a calcium-sparing diuretic that enhances calcium reabsorption
60
Q

Cystine Nephrolithiasis

A
  • a rare form of kidney stone that most commonly presents in children
  • associated with cystinuria, an autosomal recessive tubule defect resulting in poor cysteine reabsorption as well as poor reabsorption of ornithine, lysine, and arginine
  • the urine crystals are hexagonal
  • may form a radiopaque staghorn calculi
  • treatment involves hydration and alkalinization of urine
61
Q

Urinary Tract Infection

A
  • before 6 months of age, most common in uncircumcised males followed by circumcised, followed by females
  • E. coli is the primary pathogen involved by Klebsiella, Pseudomonas, Staph saprophytic, Serratia, Proteus, and Enterococcus are all common
  • in neonates, symptoms include lethargy, fever, irritability, and jaundice, but in older infants symptoms include fever, vomiting, and irritability
  • young children who are toilet-trained may present with nocturnal enuresis or daytime wetting
  • older children with cystitis may present with dysuria, urinary frequency, or urgency and a low grade fever
  • urine culture is the gold standard: infants require suprapubic aspiration or sterile urethral catheterization but older children can obtain a clean catch urine sample
  • urine culture is considered positive for any growth with suprapubic aspiration, more than 10K colonies by sterile cath, and more than 50K colonies by clean-catch
  • UA is also likely to find leukocytes or a positive nitrite or leukocyte esterase test
  • imaging is only indicated in children with pyelonephritis, recurrent UTI, males, and girls younger than 4 years old
  • treat with empiric antibiotics (usually TMP-SMX or cephalexin) in most cases; but neonates should be admitted for IV ampicillin and gentamicin; toxic-appearing children should receive IV antibiotics and fluids until improving at which point oral antibiotics can be used
  • 7-10 days of antibiotics are used for cystitis; 14 days for pyelonephritis in addition to 3 months of low-dose prophylactic antibiotics
62
Q

Cystitis

A
  • a infection fo the bladder
  • most often due to E. coli; Staph saprophyticus is characteristically seen in young, sexually active women; K. pneumoniae is a common agent; Proteus mirabilis is likely if the urine is alkaline with an ammonia scent
  • presents with dysuria, urinary frequency, urgency, and suprapubic pain, but systemic symptoms are absent
  • urine is cloudy with WBC, dipstick is positive for leukocyte esterase and nitrites, culture grows greater than 100K colonies
  • sterile pyuria (cystitis with a negative urine culture) suggests urethritis due to Chlamydia trachoma’s or Neisseria gonorrhoeae
63
Q

Acute Pyelonephritis

A
  • an infection of the kidney
  • usually due to ascending infection secondary to vesicoureteral reflux
  • presents with fever, flank pain, WBC casts, and leukocytosis in addition to the symptoms of cystitis
  • most commonly due to E. coli, Enterococcus faecalis, or Klebsiella
64
Q

Chronic Pyelonephritis

A
  • recurrent pyelonephritis, usually due to vesicoureteral reflux or obstruction
  • leads to interstitial fibrosis and atrophy of the tubules
  • atrophic tubules contain eosinophilic proteinaceous material and resemble thyroid follicles (referred to as thyroidization of the kidney)
  • cortical scarring at the upper and lower poles with blunted calyces is indicative of vesicoureteral reflux

Pediatrics BRS (20 decks)

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