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Nephro > NEPHRO > Flashcards

NEPHRO Flashcards

1
Q

definition of hematuria

A

presence of at least 5 RBCs per microliter of urine

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2
Q

Heme positive without RBCs

A

presence of myoglobin or hemoglobin

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3
Q

hematuria within the glomerulus

A

brown, cola or tea-colored or burgundy urine
protenuria >100mg/dl via dipstick
RBC casts
deformed urinary RBCs (acanthocyte)

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4
Q

hematuria arising from lower urinary tract

A 
gross hematuria, bright red or pink
terminal hematuria
blood clots
normal unrinary RBC morphology
minimal proteinuria on dipstick (<100mg/dL)
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5
Q

tea or cola colored urine, facial or body edema, hypertension and oliguria

A

acute nephritic syndrome

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6
Q

what is the most common cause of gross hematuria

A

bacterial urinary tract infection

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7
Q

urethral bleeding in the absence of urine associated with dysuria and blood spots on underwear after voiding which occurs in prepubertal boys

A

Urethrorrhagia

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8
Q

most common chronic glomerular disease

A

IgA nephropathy (Berger disease)

*IgA deposits in mesangium often accompanied by C3 complement

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9
Q

diagnosis of IgA nephropathy requires

A

renal biopsy

*mesangial proliferation that may be associated with epithelial cell crescent formation and sclerosis

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10
Q

what are the clinical manifestations of IgA nephropathy

A

gross hematuria often occurs 1-2 days of onset of an URTI or GI infection

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11
Q

C3 level in IgA nephropathy is

A

normal

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12
Q

primary treatment of IgA nephropathy

A

appropriate BP control

*other treatment: ACE inhibitors and ARB effective in reducing proteinemia and retarding rate of disease progression

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13
Q

Alport syndrome is caused by mutations in

A

genes coding for Type IV collagen

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14
Q

electron miscroscopy findings in Alport syndrome

A

diffuse thickening, thinning, splitting and layering of the glomerular and tubular basement membranes

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15
Q

what are the clinical manifestations of Alport Syndrome

A

single or recurrent gross hematuria after URTI
progressive proteinuria exceeding 1g/24hr
bilateral sensorineural hearing loss
ocular abnormalities including anterior lenticonus, macular flecks and corneal erosions

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16
Q

pathognomonic of Alport syndrome

A

anterior lenticonus

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17
Q

sudden onset of gross hematuria, edema, hypertension and renal insufficiency

A

Acute Poststreptococcal Glomerulonephritis

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18
Q

immunofluorescence microscopic findings in patients with PSGN

A

“lumpy bumpy” deposits of immunoglobulin and complement on the GBM and mesangium

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19
Q

C3 levels in PSGN

A

low

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20
Q

nephritogenic strain in PSGN

A

Group A streptococcus which posses M protein

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21
Q

patient develop acute nephritic syndrome after ___ weeks after streptococcal pharyngitis and ___ weeks after streptococcal pyoderma

A

1-2 weeks after pharyngitis

3-6 weeks after pyoderma

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22
Q

acute phase of PSGN resolves within

A

6-8 weeks

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23
Q

commonly elevated after streptococcal pharyngitis

A

ASO

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24
Q

best single antibody titer to document cutaneous streptococcal infection

A

anti-DNAse B level

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25
Q

treatment for PSGN

A

10 day course of Penicillin recommended to limit spread of nephritogenic organisms, antibiotic therapy does not affect the natural history of GN

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26
Q

most common cause of membranous glomerulopathy worldwide

A

Malaria

  • diffuse thickening of the GBM without significant cell proliferative changes
  • in situ immune complex formation
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27
Q

treatment for Membranous Glomerulopathy

A

Immunosuppressive therapy

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28
Q

also known as mesangiocapillary glomerulonephritis

A

Membranoproliferative GN

  • most common in 2nd decade of life
  • C3 levels remains persistently low
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29
Q

most common type of MPGN

A

Type I

  • glomeruli have accentuated lobular pattern from diffuse mesangial expansion
  • crescents if present signify poor prognosis
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30
Q

indications for renal biopsy

A

nephrotic syndrome in an older child
significant proteinuria with microscopic hematuria
hypocomplementemia lasting >/=2 months in a child with acute nephritis

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31
Q

most important cause of morbidity and mortality in SLE

A

Glomerulonephritis

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32
Q

minimal mesangial lupus nephritis

no histologic abnormalities on light microscopy but mesangial immune deposits are present on IF or EM

A

WHO Class I nephritis

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33
Q

mesangial proliferative nephritis

A

WHO Class II nephritis

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34
Q

proliferative nephritis; <50% glomeruli involvement

A

WHO Class III nephritis

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35
Q

proliferative nephritis; >50% glomeruli involvement

A

WHO Class IV nephritis

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36
Q

membranous lupus nephritis

A

WHO Class V nephritis

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37
Q

therapy given in Lupus nephritis

A

Prednisone

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38
Q

may be given in WHO Class I or II Lupus nephritis

A

Azathioprine

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39
Q

most common small vessel vasculitis

A

HSP

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40
Q

clinical manifestations of HSP

A

purpuric rash
arthritis
abdominal pain

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41
Q

when should urinalysis be requested in patients with HSP?

A

weekly in patients with HSP during period of active clinical disease and once a month for up to 6 months thereafter

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42
Q

when should treatment be given to patients with HSP nephritis?

A

severe HSP nephritis

>50% crescents on biopsy

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43
Q

hallmark of Rapidly progressive GN

A

crescents in glomeruli

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44
Q

characterized by pulmonary hemorrhage and glumerulonephritis

A

Goodpasture Disease

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45
Q

treatment for Goodpasture disease

A

high dose IV methylpred, cyclophosphamide and plasmapharesis

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46
Q

triad of HUS

A

renal insufficiency
thrombocytopenia
microangiopathic hemolytic anemia

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47
Q

most common cause of HUS

A

toxin-producing E. coli that cause prodromal acute enteritis

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48
Q

what are the early glomerular changes in HUS

A

thickening of capillary walls caused by swelling of endothelial cells and accumulation of fibrillary material between endothelial cells and underlying basement membrane causing narrowing of capillary lumen

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49
Q

characteristic of all forms of HUS

A

microvascular injury

endothelial cell damage

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50
Q

prognosis in HUS

A

those with HUS not associated with diarrhea is more severe

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51
Q

common causes of renal vein thrombosis in infants and newborn

A 
asphyxia
dehydration
shock
sepsis
congenital hypercoaguable state
maternal diabetes
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52
Q

common causes of renal vein thrombosis in older children

A 
nephrotic syndrome
cyanotic heart disease
inherited hypercoaguable state 
sepsis
following kidney transplantation
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53
Q

sudden onset of gross hematuria and unilateral or bilateral flank mass

A

Renal vein thrombosis

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54
Q

primary treatment for renal vein thrombosis

A

supportive care
correction of fluid and electrolytes
treatment of renal insufficiency

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55
Q

treatment for patients with thrombosis of inferior vena cava

A

can require surgical thrombectomy

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56
Q

triad of nephrotic syndrome

A

hypoalbuminemia
edema
hyperlipidemia

57
Q

nephrotic range proteinuria

A

protein excretion >40mg/m2/hr or

1st morning protein:creatinine ratio >2-3:1

58
Q

findings on kidney biopsy in patients with nephrotic syndrome

A

extensive effacement of foot process

Hallmark of nephrotic syndrome

59
Q

important features of minimal change idiopathic nephrotic syndrome

A

absence of hypertension and gross hematuria

60
Q

treatment for minimal change disease

A

6 weeks course of daily steroid treatment

61
Q

steroid resistant is defined as

A

children who continue to have proteinuria (2+ greater) after 8 weeks of steroid therapy –> diagnostic biopsy should be performed

62
Q

normal anion gap (hyperchloremic) metabolic acidosis

A

Renal tubular acidosis

63
Q

proximal RTA is also called

A

Type II

  • fanconi syndrome
  • cystinosis
  • Lowe syndrome: congenital cataracts, mental retardation and Fanconi
64
Q

what are the manifestations of Fanconi syndrome

A 
LMW proteinuria
glycosuria
phosphaturia
aminoaciduria
proximal RTA
65
Q

manifestations of Type II RTA

A

growth failure in the 1st year of life

Urine pH is acidic (<5.5) because distal acidification mechanism is intact

66
Q

distal RTA is also called

A

Type I RTA

67
Q

what happens in distal RTA?

A

impaired hydrogen ion excretion hence urine PH cannot be reduced to <5.5 despite presence of acidosis

  • hypokalemia
  • hypercalciuria
68
Q

RTa type IV is also known as

A

Hyperkalemic RTA

*impaired aldosterone production or impaired renal responsiveness to aldosterone

69
Q

blood anion gap <12

A

absence of anion gap

70
Q

blood anion gap >20

A

highly suggestive of presence of anion gap

71
Q

positive anion gap suggests deficiency of

A

ammoniagenesis

72
Q

negative anion gap is consistent with

A

proximal tubule bicarbonate wasting (GI bicarbonate wasting)

73
Q

mainstay of treatment in all forms of RTA

A

bicarbonate replacement

74
Q

urine shows elevated SG (>1.020), elevated urine osmolality (UOsm >500mOsm/kg), low urine NA <20meq/L, fractional excretion of sodium (FENa <1%)

A

prerenal ARF

75
Q

urine shows SG (<1.010), low urine osmolality (UOsm <350 mOsm/kg), high urine NA >40meq/L, fractional excretion of sodium (FENa >2%)

A

intrinsic ARF

76
Q

indications for dialysis in ARF

A

volume overload with evidence of hypertension and/or pulmonary edema
persistent hyperkalemia
severe metabolic acidosis unresponsive to medical tx
neurologic symptoms
BUN >100-150 mg/dl
Calcium:phosphorus imbalance with hypocalcemic tetany

77
Q

principal extracellular cation

A

Sodium

78
Q

principal intracellular cation

A

Potassium

79
Q

positive water balance –> decreased osmolality

A

hyponatremia

80
Q

negative water balance –> increased osmolality

A

hypernatremia

81
Q

factors that promote potassium secretion

A
  1. Aldosterone
  2. Increased Na delivery to the distal nephron
  3. increased urinary flow rate
82
Q

role of kidney in acid-base balance:

reabsorption of HCO3

A

proximal tubule

83
Q

role of kidney in acid-base balance:

secretion of H+ as titratable acid and ammonium

A

Distal tubule

84
Q

characteristics of Renal tubular disorders

A
  • usually inherited
  • affected children have growth failure
  • some disorders are benign and require no therapy
  • disorders may be treated with replacement of substance being lost in the urine or removal of an offending substance or metabolite
85
Q

presence of anion gap

A

> 20
lactic acidosis
inborn errors of metabolism
ingestions

86
Q

urine anion gap <0

A

RTA type II proximal

87
Q

Urine anion gap >0

A

RTA Type I

RTA Type IV

88
Q

what are the manifestations of distal RTA (Type I)?

A

vomiting, failure to thrive, acidosis ( more severe than RTA)
Nephrocalcinosis
renal calculi
bone disease –>rickets or osteomalacia

  • nephrocalcinosis
  • hyperchloremia
  • hypercalciuria
89
Q

what is Bartter syndrome?

A

*rare form of hypokalemic metabolic alkalosis with hypercalciuria
*mutation in Na-K-Chloride contransporter
*2 types:
Antenatal
Classic
*damage at thick ascending limb
*severe hypokalemia <2.5mmol/L with metabolic acidosis

90
Q

damage at thick ascending limb

A

Bartter syndrome

91
Q

treatment for Bartter syndrome

A

*prevent/correct dehydration
*potassium supplementation –> 1-3 mEq/kg/day
*Administration of Indomethacin (type 2 are sensitive)
Type 4 resistant to Indomethacin
*Spinorolactone 10-15mg/kg/day
*may lead to chronic renal failure

92
Q

What is Gitelman’s syndrome

A
  • familial hypokalemia-hypomagnesemia
  • much common in adult
  • involves thiazide-sensitive co-transporter located in DCT; diminished NaCl transport in DCT
  • often asymptomatic
  • transient episodes of tetany and weakness usually associated with abdominal pain, vomiting and fever
  • salt-craving, musculoskeletal symptoms, constitutional symptoms
  • growth retardation is absent
93
Q

Treatment for Gitelman’s syndrome

A

best treated with Mg salts alone

94
Q

inability to concentrate urine

A

Nephrogenic Diabetes Insipidus

  • damage to collecting tubule
  • resistant to ADH
  • presents soon after birth
  • poor appetite, vomiting, FTT due to excessive water intake
  • massive polyuria, hypernatremia, volume depletion, hyperthermia, polydipsia
95
Q

laboratory findings in Nephrogenic Diabetes Insipidus

A
  • polyuria: UO >2000ml/m2/day or 40ml/kg/day
  • serum osmolality: >290 mOsm/kg
  • urine osmolality: <290 mOsm/kg
  • increased serum osmolality
  • decreased serum osmolality
96
Q

Definition of normal BP

A

Children 1-13: <90th percentile for age, sex, height

Children >/=13: <120/ <80 mmHg

97
Q

definition of elevated BP

A

Children 1-13: >90th to <95th percentile for age, sex, height
Children >/=13: 120/<80 mmHg

98
Q

definition of Stage 1 hypertension

A

Children 1-13: >95th to <95th percentile + 12mmHg or 130/80 to 139/89 mmHg (whichever is lower)
Children >/=13: 130/80 to 139/89

99
Q

definition of Stage 2 hypertension

A

Children 1-13: >95th + 12mmHg or >/=140/90mmHg (whichever is lower)
Children >/=13: >/=140/90 mmHg

100
Q

BP should be checked starting at what age

A

3 years old

101
Q

correct BP cuff size

A
  • bladder width: approx 40% of the circumference of upper arm midway between olecranon and acromion
  • bladder length: should encircle 80-100% of the circumference of upper arm
102
Q

how to use the normative BP table

A

Step 1: recognition of elevated BP

  • should be checked 3x then get average
  • determine height percentile of the child using CDC growth chart
  • use correct gender table for SBP and DBP

Step 2: evaluation of etiology
evaluate comorbidities, screen for evidence of target organ damage

103
Q

screening tests for all patients with elevated BP

A

Urinalysis
BUN, Crea,
Lipid profile
Renal ultrasound

104
Q

screening tests for obese BMI >95th percentile or adolescent

A

HBA1c
AST and ALT
Fasting lipid panel

optional: 
Fasting serum glucose
DM
TSH
Drug screen
Sleep study
CBC especially those with growth delay or abnormal renal function
105
Q

screening tests for patients with comorbid factors and BP 90th to <95th percentile; all patients with BP >/= 95th percentile

A

evaluate for target-organ damage:

Echocardiogram to identify LVH
retinal exam

106
Q

screening test for all children with persistent BP >/=95th percentile

A

ambulatory BP monitoring (ABPM)

107
Q

mainstay of therapy for children with asymptomatic mild hypertension without evidence of target-organ damage

A

Lifestyle modification

108
Q

primary therapy in obesity-related hypertension

A

weight loss

109
Q

recommended diet for adolescents and adults

A 
DASH diet 
decrease sodium intake
increase potassium, calcium and magnesium containing foods
6-8 servings of whole grains/ day
4-5 servings of fruits/day
4-5 servings of vegetables/day
low fat dairy food
110
Q

risk factors for UTI

A 
female gender
uncircumcised male
vesicoureteral reflux
toilet training
voiding dysfunction
obstructive uropathy
urethral instrumentation
sources of external irritation
constipation
anatomic abnormality
neuropathic bladder
sexual activity
pregnancy
111
Q

diagnosis of UTI in culture results

A

*shows >50,000cfu/ml
*single pathogen (suprapubic or catheter sample) +
UA has pyuria or bacteriuira in a symptomatic child =UTI
*in bag sample, if UA (+), patient symptomatic –> catheter sample should be obtained –> CS

112
Q

treatment for acute cystitis

A

mild or diagnosis doubtful: tx can be delayed
if tx indicated: 3-5 day course of TMP-SMX (6-12 TMP/kg/day in 2 divided doses)
Nitrofurantoin (5-7mg/kg/24hr) effective in Kleb and Enterobacter
Amoxicillin (50mg/kg/24hr) in 2 divided doses

113
Q

treatment for pyelonephritis

A

Acute Febrile UTI (7-14 days)

hospitalized: Ceftriaxone 50mg/kg/24hr or Cefepime or Cefotaxime
* Nitrofurantoin should not be used routinely in children -with febrile UTI- no significant tissue levels
* repeat urine CS not routinely needed after termination of treatment

114
Q

“bottom up” approach

A

renal sonogram plus VCUG

115
Q

“top down” approach

A

DMSA scan –> if (+) –> VCUG

116
Q

risk factors for recurrent UTI

A

age
vesicoureteral reflux
bowel bladder dysfunction

117
Q

Mainstay therapy in all forms of RTA

A

Bicarbonate replacement

118
Q

Hypokalemic hypochloremic metabolic alkalosis with hypercalciuria and salt wasting

A

Bartter syndrome

119
Q

Optimal therapy for children with ESRD

A

Kidney transplantation

120
Q

Most common complication of nephrotic syndrome

A

Infection

121
Q

In patients with isolate microscopic hematuria who are asymptomatic, what should be done?

A

Obtain atleast 3 urinalysis at 2 week period then if hematuria persists, it should be evaluated

Annual creatinine with BP monitoring

122
Q

most common cause of gross hematuria

A

bacterial UTI

123
Q

most common chronic glomerular disease in children

A

IgA nephropathy

124
Q

most common cause of persistent proteinuria in school age and adolescents

A

Orthostatic (postural) proteinuria

125
Q

most common presenting symptom of children with nephrotic syndrome

A

Edema

126
Q

most common form of glomerulonephritis

A

Postinfectious GN

127
Q

most common form of HUS

A

diarrhea associated HUS from E. coli

128
Q

most common serious bacterial infection in infants <24 months with fever without an obvious focus

A

Pyelonephritis

129
Q

most common characteristic of urinary tract obstruction

A

hydronephrosis

130
Q

most common cause of severe obstructive uropathy

A

posterior urethral valves

131
Q

most common cause of daytime incontinence

A

overactive bladder

132
Q

sign of urethral prolapse

A

bloody spotting on underwear or diaper

133
Q

most common tumor developing in an undescended testis in an adolescent or adult

A

Seminoma

134
Q

most common foreign object causing vaginal bleeding in prepubertal girls

A

toilet paper

135
Q

most common obstructive anomaly of the vagina

A

imperforate hymen

136
Q

most common cause of vaginal agesis

A

Mayer-Rokitansky-Kuster-Hauser syndrome

137
Q

most common Mullerian anomaly

A

uterine septum

138
Q

bilateral palpable flank masses in an infant with pulmonary hypoplasia, oligohydramnios, and hypertension and the absence of renal cysts by sonography of the parents

A

ARKPD

Nephro (1 decks)

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