Volume 1 Flashcards

(63 cards)

1
Q

criteria for SIADH

A
  1. Absence of: Renal, adrenal, or thyroid insufficiency Heart failure, nephrotic syndrome, or cirrhosis, Diuretic, ingestion, Dehydration 2. Urine osmolality > 100 mOsm/kg (usually > plasma) 3. Serum osmol< 280 mOsm/kg and serum Na < 135 mEq/L 4. Urine sodium > 30 mEq/L 5. Reversal of “sodium wasting” and correction of hyponatremia with water restriction
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2
Q

SFU grading

A

Grade 0 − Normal examination with no dilatation of the renal pelvis Grade I − Mild dilatation of the renal pelvis only (image 2) Grade II − Moderate dilatation of the renal pelvis including a few calyces Grade III − Dilatation of the renal pelvis with visualization of all the calyces, which are uniformly dilated, and normal renal parenchyma Grade IV − Similar appearance of the renal pelvis and calyces as Grade III + thinning of the renal parenchyma

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3
Q

what is Bartter syndrome?

A

very rare, like giving someone too much lasix met alkalosis, Low K HIGH urine Ca polyuria

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4
Q

what are the main categories of hematuria?

A
  1. Vascular - renal vein thrombosis, vasculitis, AVM, loin pain-hematuria syndrome
  2. glomerular -MC, GN(IgA, post strep, HSP…)
  3. tubulointerstitial
  4. lower tract
  5. caogulation
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5
Q

what is Alport syndrome?

A

X linked dominant

mutation of collagen 4

  1. hematuria
  2. proteinuria
  3. HTN
  4. progressive SNHL
  5. eye invol - ant lenticonus, macular flecks, corneal erosiso
  6. plt issues
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6
Q

what is the prognosis for Alport syndrome?

A

THe amount of protein and Fhx

Male - HTN, ESRD by 30, gradual hearing loss

Females - mild disesase but still ESRD but later

Weather AD or AR - still get ESRD

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7
Q

what are poor prognostic factors for Alport Syndrome?

A
  1. gross hematuria
  2. dev NEPHROTIC syndrome
  3. prominent BM thickness
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8
Q

what is the pathophys of post strep GN

A

immune complex mediated GN

(Ag-Ab complment activation)

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9
Q

what is the CP of post strep GN

A
  1. macro hematuria + casts
  2. proteinuria
  3. edema
  4. HTN
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10
Q

when does post strep GN present

A

1-3 weeks post throat of skin infcetion

95% recover within 3-4 weeks

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11
Q

What are the lab values that can help Dx post strep GN

A
  1. high ASOT/AntiDNAse B
  2. Normal C4
  3. LOW C3
  4. =-BUN/creat
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12
Q

which GN have hypocomplementia?

A

post infectious

SLE

membranoproliferative

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13
Q

what BW can help you diagnoses HSP?

A

none

only helps rule out other things

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14
Q

what is the management of Alports syndrome

A

most require transplant in their lifetime

can get Ab against normal collagen 4 from transplant leading to regection or Goodpasture’s

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15
Q

what are CP of HSP

A
  1. CNS: Sz, encephalitis
  2. resp - could have some hemmorrhage but very rare
  3. Skin - palpable purpura, pitting/non pit edema
  4. GI:bleeding/edma, PAIN, intuss, ischemia
  5. Jt: migatory polyarthritis
  6. Kidneys - hematuria, proteinuria, HTN, can progress
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16
Q

what are diagnostic criteria for HSP

A
  1. palpable purpura + at least 1
    1. abdominal pain
    2. arthritis or arthralgia
    3. renal involvment - heme or proteinuria
    4. inc IgA on Bx
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17
Q

what percentage of patient with EColi 0157:H7 dvelop HUS

A

10%

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18
Q

what are CP of HUS

A
  1. microangiopathic hemolytic (Coombs neg) anemia
  2. LOW plt
  3. Renal failure
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19
Q

what are the causes of HUS

A
  1. Typical: with diarrhea D+. E.coli 0157:H7, shigella
  2. Atypical: D - = drugs, malignancy, infectious strep pneumo, HIV, pregnancy, collagen vascular disease, genetics. WORST outcomes, SLE, strep pneumo,
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20
Q

what are the lab findings for HUS?

A
  1. anemia - schistocytes and helmet cells on smear reflecting mechanical trauma within vessels
  2. Thrombocytopenia
  3. normal coag
  4. high D-dimers
  5. DAT/coombs neg
  6. high bili and LDH
  7. if have gi issues - high amylase, lipase, high LFTs
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21
Q

what are causes of calcium stones?

A
  1. Familial idiopathic hypercalciuria
  2. High Vit D - inc intestinal Ca absorption
  3. Endo - hypothyroid, hyperparathyroid
  4. Bone issues - immobilization, rickets, malign, JIA
  5. hyperoxacaluria, hypocitraturia
  6. iatrogenic - loop diuretic, ketogenic diet, steroids, theophyline
  7. Williams syndrome
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22
Q

what are causes of struvite stones

A
  1. urea splitting org UTI - proteus
  2. foereign body
  3. urinary stasis
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23
Q

what are causes of uric acid stones?

A
  1. tumour lysis
  2. chemotherapy
  3. IBD
  4. Lesch-Nylan syndrome
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24
Q
  1. what causes xanthine stones?
  2. What causes Cystine stones?
A
  1. allopurinol, xanthinuria
  2. cystinosis, cystinuria
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25
what is the work up for renal stone
1. Serum - uric acid, K, Cr, Ca, PO4, urea, creat and ALP 2. Urine - UA, cult, Ca:crea ratio, cystine, 24hr urine collection 3. If hypercalciuria, hypercalcemia or hypoPO4 - do PTH
26
what can be associated with large placenta
neonatal nephrotic syndrome
27
what are the features of nephrotic syndrome
1. dependent edema - ususally 1st sign 2. proteinuria 3. Low Albumin \< 25 d/L 4. High Cholesterol \>250mg/Dl, 5. high TGL, 6. high lipoproteins 7. hypovolemia and high creat 8. HTN 9. N/V/D 10. funsctional asplenia bc lose complements
28
What is FeNa?
_Urine Na x Plasma Crea_ Plansma Na X Urine creat ===== U pee Na
29
when do you use FeNa
1. helps figure out if pre renal vs post renal - important in NS to figure out if underfilled 2. pre-renal \< 1 3. renal if \> 2 = intrinsic renal issue
30
What are false positives for hematuria
1. dyes 2. rifampin 3. myoglobulin 4. menstruation 5. alkalinize urine 6. cleaning solutions
31
autosomal recessive PKD
1. presents - oligohydramnios, lung hypoplasia... 2. abdno mass 3. HTN 4. polyuria 5. hepatic fibrosis, 6. Biliary issues 7. mortality 30 % from resp
32
autosomal Dominant PCK
1. Brain aneurysm 2. mitral valve prolaps
33
What are causes for glomerular proteinuria?
large and small molecular wgty prot + Glomerular disease (hematuria, RBC catsa, HTN, renal insuff) EG: HUS, PSGN, lupus nephritis, congenital NS
34
What are mgnt options for NS
1. STEROIDS - even without Bx if typical features. Pred 2mg/kg/day. 2. low salt or no added salt 3. acute HTN - Beta bloc or Ca channel, chronic -ACEi 4. Loop diuretic 5. monitor for infections
35
what are complications of NS
1. infection - strep pneumo, E.Coli, Klebsiella due to loss of Ib and Complements 2. SE of steroids 3. hypovolemia 4. hypercoagulable state - loss of Coag factors, anti thrombin, plasminogen 5. atherosclerosis
36
what % of MCNS will experience a relapse?
80% and respond well to treatment can have transient proteinuria with intercurrent infections
37
How do glomerulonephritis present
1. hematuria + casts 2. edema 3. HTN 4. proteinuria 5. oligouria 6. renal insuff
38
how can you differenciate glomerular from tubulointerstitial GN
1. Glomerular - hematuria, proteinuria, edema, HTN, renal insiff 2. Tubulo - mild proteinuria, no HTN, impaired H2O handling
39
what is the most common chronic GN
IgA nephropathy
40
what would be your differential if child has hematuria during a viral URTI?
IgA nephropathy - more common in boys
41
What is the FENa formula
_Urine Na x Plasma Creat_ Urine Creat x Na plasma
42
what UA analysis might tell you this is pre-renal insifficiency?
1. Serum BUN/Creat \> 20 2. FeNa \< 1 3. U osm \>500 4. Urine Na \< 20
43
what UA analysis might tell you this is RENAL insifficiency?
1. FeNa \> 2 2. serum BUN/Creat 10 ish 3. Urine osm 300 ish 4. Urine Na \> 40 -high
44
how do you manage hyperkalemia
1. Ca IV to protect the heart 2. Bicarbonate for the acidosis 3. beta agonists - ventolin 4. glucose and insulin 5. diurectics dialysis
45
what is RTA?
inappropriately alkaline urine in the presence of serum acidosis, normal AG, and normal GFR
46
what is proximal RTA
type II: •Decreased tubular threshold for _reabsorption_ of HCO; therefore HCO3 wasting •H+ secretion intact •If given bicarb, will develop massive bicarbonaturia, but can correct acidosis
47
what is distal RTA?
Type 1: LOW K and HIGH Ca * Inability of distal tubule to secrete H+ * Usually more severe acidosis than type II
48
what is type 4 RTA
* Five different subtypes; * basically decreased aldosterone or decreased sensitivity to aldosterone
49
what are complications of nephrotic syndrome?
1. increased risk of infection 2. hypercoagulable - decreased intravascular and dec antithrombin III
50
what is the DDX for nephrotic ange proteinuria
1. minimal change NS 2. focal segmental glomerulosclerosi 3. congenital NS
51
who gets minimal change NS
1. 2-6 yrs 2. males 3. especially if \< 7 yrs
52
what children with presumed MGNS require a Bx
1. if \< 1 yrs -? congenital 2. if \> 12 yrs - ? membranous 3. if black - could be SLE 4. If no response to steroid at 4 weeks 5. if RF 6. if macrohematuria 7. if microhematuria + HTN during remission
53
what small proteins are lost in NS
1. albumin 2. IgG 3. antithrombin III 4. protein C/S
54
what large proteins are increasedin NS
1. IgM 2. fibrinogen 3. beta lipoproteins
55
what is a worrying sign in NS presentation?
1. Hypovolemia - higher rates of mortality need to clarify is underfilled or overfilled!
56
if you are unsure if a pt with NS is under or over filled, what will help?
1. FeNa \< 1 = underfilled 2. urine K/ urine Na+K - if \> 60% = underfilled
57
when do you treat hypercholesteroemia in NS
1. if albumin remains persistently low and 2. if poor response to traetment
58
what is the steroid magnt of NS
1. ›60 mg/m2/day divided tid X 6 wks, then 2. ›40 mg/m2 q2d (in one dose) X 6 wks, then stop
59
when should NS pt respond to Rx
* within first 2 weeks * need to complete 4 weeks before can say they are resistant
60
if NS pt does not respond after 1st treatment, what do you do?
1. repeat steroid course or 2. ›Cyclophosphamide (IV or po) 3. ›Mycophenolate Mofetil (MMF) 4. ›Maintenance Prednisone of 0.1-0.5 mg/kg/alt day (for 6-12 months)
61
what are the 2 types of FSGS ( NS)
1. primary - more common in childre 2. secondary - adults eg. HIV, sickle cell, hep B, SLE, obesity
62
how does FSGS progress
ofetn steroid resistant 1/3 to ESRD 1/3 need transplant
63
what is a concerning lab finding for a patient with NS?
low C3 - because could be MPGN which has worse outcome