Volume 1 Flashcards

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
Q

what is the work up for renal stone

A
  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
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26
Q

what can be associated with large placenta

A

neonatal nephrotic syndrome

27
Q

what are the features of nephrotic syndrome

A
  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
Q

What is FeNa?

A

Urine Na x Plasma Crea

Plansma Na X Urine creat

===== U pee Na

29
Q

when do you use FeNa

A
  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
Q

What are false positives for hematuria

A
  1. dyes
  2. rifampin
  3. myoglobulin
  4. menstruation
  5. alkalinize urine
  6. cleaning solutions
31
Q

autosomal recessive PKD

A
  1. presents - oligohydramnios, lung hypoplasia…
  2. abdno mass
  3. HTN
  4. polyuria
  5. hepatic fibrosis,
  6. Biliary issues
  7. mortality 30 % from resp
32
Q

autosomal Dominant PCK

A
  1. Brain aneurysm
  2. mitral valve prolaps
33
Q

What are causes for glomerular proteinuria?

A

large and small molecular wgty prot + Glomerular disease (hematuria, RBC catsa, HTN, renal insuff)

EG: HUS, PSGN, lupus nephritis, congenital NS

34
Q

What are mgnt options for NS

A
  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
Q

what are complications of NS

A
  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
Q

what % of MCNS will experience a relapse?

A

80% and respond well to treatment

can have transient proteinuria with intercurrent infections

37
Q

How do glomerulonephritis present

A
  1. hematuria + casts
  2. edema
  3. HTN
  4. proteinuria
  5. oligouria
  6. renal insuff
38
Q

how can you differenciate glomerular from tubulointerstitial GN

A
  1. Glomerular - hematuria, proteinuria, edema, HTN, renal insiff
  2. Tubulo - mild proteinuria, no HTN, impaired H2O handling
39
Q

what is the most common chronic GN

A

IgA nephropathy

40
Q

what would be your differential if child has hematuria during a viral URTI?

A

IgA nephropathy - more common in boys

41
Q

What is the FENa formula

A

Urine Na x Plasma Creat

Urine Creat x Na plasma

42
Q

what UA analysis might tell you this is pre-renal insifficiency?

A
  1. Serum BUN/Creat > 20
  2. FeNa < 1
  3. U osm >500
  4. Urine Na < 20
43
Q

what UA analysis might tell you this is RENAL insifficiency?

A
  1. FeNa > 2
  2. serum BUN/Creat 10 ish
  3. Urine osm 300 ish
  4. Urine Na > 40 -high
44
Q

how do you manage hyperkalemia

A
  1. Ca IV to protect the heart
  2. Bicarbonate for the acidosis
  3. beta agonists - ventolin
  4. glucose and insulin
  5. diurectics dialysis
45
Q

what is RTA?

A

inappropriately alkaline urine in the presence of serum acidosis, normal AG, and normal GFR

46
Q

what is proximal RTA

A

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
Q

what is distal RTA?

A

Type 1:

LOW K and HIGH Ca

  • Inability of distal tubule to secrete H+
  • Usually more severe acidosis than type II
48
Q

what is type 4 RTA

A
  • Five different subtypes;
  • basically decreased aldosterone or decreased sensitivity to aldosterone
49
Q

what are complications of nephrotic syndrome?

A
  1. increased risk of infection
  2. hypercoagulable - decreased intravascular and dec antithrombin III
50
Q

what is the DDX for nephrotic ange proteinuria

A
  1. minimal change NS
  2. focal segmental glomerulosclerosi
  3. congenital NS
51
Q

who gets minimal change NS

A
  1. 2-6 yrs
  2. males
  3. especially if < 7 yrs
52
Q

what children with presumed MGNS require a Bx

A
  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
Q

what small proteins are lost in NS

A
  1. albumin
  2. IgG
  3. antithrombin III
  4. protein C/S
54
Q

what large proteins are increasedin NS

A
  1. IgM
  2. fibrinogen
  3. beta lipoproteins
55
Q

what is a worrying sign in NS presentation?

A
  1. Hypovolemia - higher rates of mortality

need to clarify is underfilled or overfilled!

56
Q

if you are unsure if a pt with NS is under or over filled, what will help?

A
  1. FeNa < 1 = underfilled
  2. urine K/ urine Na+K - if > 60% = underfilled
57
Q

when do you treat hypercholesteroemia in NS

A
  1. if albumin remains persistently low and
  2. if poor response to traetment
58
Q

what is the steroid magnt of NS

A
  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
Q

when should NS pt respond to Rx

A
  • within first 2 weeks
  • need to complete 4 weeks before can say they are resistant
60
Q

if NS pt does not respond after 1st treatment, what do you do?

A
  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
Q

what are the 2 types of FSGS ( NS)

A
  1. primary - more common in childre
  2. secondary - adults eg. HIV, sickle cell, hep B, SLE, obesity
62
Q

how does FSGS progress

A

ofetn steroid resistant

1/3 to ESRD

1/3 need transplant

63
Q

what is a concerning lab finding for a patient with NS?

A

low C3 - because could be MPGN which has worse outcome