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Nephro > high yield > Flashcards

high yield Flashcards

1
Q

major function of ADH

A

insert water channels into collecting duct luminal surface to increase water reabsorption (w/o ADH collecting duct is impermeable to water)
released from supraoptic nuclei in hypothalamus

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2
Q

sodium reabsorption proximal tubule

A

50-55% reabsorbed;
NH exchanger
Na–glu, aa, phos, organic solute cotransporter

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3
Q

sodium reabsorption loop of henle

A

35-45%

NKCC transporter

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4
Q

sodium reabsorption distal tubule

A

5-8%

NC cotransporter

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5
Q

sodium reabsorption collecting tubule

A

2-3%

ENAC

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6
Q

if ADH is absent, urine osmolality=?

A

<100

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7
Q

DDX of urine osmolality<100

A
  • Psychogenic Polydipsia
  • Beer Potomania (aka Tea + Toast, aka Low Osmolar Load hyponatremia)
  • Reset Osmostat (if pt’s serum Osm is below their set-point)
  • “You Fixed It” Hyponatremia (Pt with prior UOsm > 100, but cause went away)
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8
Q

hyponatremic, hypervolemic

A

CHF
cirrhosis
nephrosis

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9
Q

hyponatremic, hypovolemic

A 
GI loss
Sweating excessively
Thiazides
Cerebral Na wasting
Aldosterone deficiency
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10
Q

Hyponatremic euvolemic

A

SIADH
Glucocorticoid deficiency
hypothyroidism
reset osmostat

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11
Q

clinical symptoms of hyperkalemia

A

Cardiac: arrhythmias
o Neuromuscular: paralysis
o Renal: hyperchloremic acidosis (interferes w/ renal ammonium excretion, thereby limiting acid excretion)

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12
Q

causes of yellow/orange urine

A

concentrated urine
bile
meds (rifampin, coumadin, flaglyl)
urate

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13
Q

causes of red/brown/black urine

A

blood (RBC or Hgb)
myoglobin
meds (phenothiazines, dilantin)
Food (beets, blackberries, red dye)

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14
Q

causes of blue/green urine

A

meds (amitriptyline, methylene blue, indomethican)

pseudomonas infection

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15
Q

normal glomerulus by LM in a child with heavy proteinuria

A

minimal change disease

confirm by noting FPP (?) by EM

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16
Q

subepithelial electron dense deposits on EM

A

membranous glomerulonephritis in adults

post-strep glomerulonephritis in kids

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17
Q

subendothelial depsits

A

membranoproliferative glomerulonephritis (but check for clinical description SLE!)

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18
Q

hematuria

A

IgA neprhopathy, esp in conjunction with URI

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19
Q

history of deafness or alterations in glomerular basement membrane

A

hereditary nephritis–Alport syndrome

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20
Q

IF pattern is coarsely granular

A

post-strep glomerulonephritis

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21
Q

thickened basement membranes by EM

A

diabetetes; confirm with PAS positive material on LM

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22
Q

fibrils on EM

A

amyloidosis

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23
Q

IF pattern is linear

A

Goodpastures syndrome (anti-basement membrane disease)

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24
Q

pt has signs and symptoms of systemic disease

A

overall diagnosis–SLE, systemic vasculitis, diabetes then find secondary renal involvement

25
Q

Euvolemic hypernatremia causes

A

Renal: central or nephrogenic DI
Extrarenal: respiratory loss, dermal loss

26
Q

Hypovolemic hypernatremia

A

Renal: osmotic diuretic, loop diuretic, post-obstruction, intrinsic renal disease
Extrarenal: GI loss, burns

27
Q

Hypervolemic hypernatremia causes

A

too much salt water in system (ingestion, IV etc)

28
Q

in hyponatremia, if sodium is correct too quickly what is the risk?

A

osmotic demyelination

  • signs/sx: dysarthria, weakness, seizures,lethargy, *irreversible
  • occurs 2-6days after treatment
  • risk factors: over-correction (>12meq/24h or >0.5meq/h), females, alcoholism, malnutrtion, liver dysfx, hypokalemia
29
Q

causes of high anion gap metabolic acidosis (5)

A
  1. increased acid production (lactic acidosis, ketoacidosis)
  2. ingestion toxins (salicylate, methanol, ethylene glycol)
  3. Advanced renal failure (GFR<20)
  4. massive rhabdomyolysis
  5. septic shock
    * all others are normal anion gap
30
Q

unilateral renal agenesis

A

: asymptomatic, solitary kidney undergoes compensatory hypertrophy and performs function of missing kidney

31
Q

bilateral renal agenesis

A
  • Assoc. w/ potter’s syndrome: pulmonary hypoplasia, facial and limb abnormalities
  • Incompatible with life
  • Oligohydraminos (responsible for lung, face, limb abnormalities)
32
Q

malrotation and ectopic kidneys

A
  • Proper rotation of kidney is with hilum facing medially
  • Ectopic kidneys from failure to ascend→located in pelvis
  • These kidneys have inc. incidence of extra or malplaced ureters or blood vessels
33
Q

horseshoe kidney

A
  • Assoc. w/ Turners Syndrome
  • Fusion of lower renal poles during development; IMA limits ascent of fused kidney
  • Asymptomatic or present with urinary obstruction, abdominal mass, or hematuria from pelvic trauma or infection
34
Q

dyplastic kidney

A

Renal parenchyma comprised of cysts, immature glomeruli and tubules, undifferentiated mesenchyme and connective tissue
• May present with varying degrees of renal obstruction or insufficiency
• Non-inherited!

35
Q

polycystic kidney disease

A 
•	Inherited!
•	Bilateral enlargement
•	Cysts in renal cortex AND medulla
Autosomal recessive PKD:
•	Infants
•	Present with renal failure, HTN
•	Potters sequence
•	Congential hepatic fibrosis and cysts (portal HTN)
Autosomal dominant PKD:
•	Young adults
•	Present with HTN, hematuria, worsening renal failure
•	APKD1/2 mutations
•	Berry aneurysms, hepatic cysts, mitral valve prolapse
36
Q

medullary cystic kidney disease

A
  • Cysts in medulla (vs PKD has cysts in cortex and medulla)
  • Shrunken kidneys (vs PKD has enlarged kidneys)
  • Present with renal failure
37
Q

ectopic ureter and ureteral obstruction

A
  • Extra/ectopic/duplicated ureters can drain to anomalous locations in bladder, urethra, vagina, or ductus deferens
  • Assoc. w/ VUR
38
Q

VUR

A

retrograde movement of urine from bladder towards renal pelvis
• From anatomic and functional abnormalities of ureteres and bladder
• High risk for pyelonephritis and scarring and hypertension
• Grading: 1-5
• w/ chronic VUR, there is dilation of urters and kidneys

39
Q

physiologic differences neonate vs adult kideny

A

neonate has…

  • dec GFR
  • dec Na handling capacity (higher FENa)
  • dec concentrating ability (tubules relatively insensitive to ADH, and lack of medullary hypertonicity)
  • dec. ability to reabsorb bicarb
40
Q

obtaining pediatric urine sample for urinalysis

A

o Clean catch: ideal for continent patients
o Bag specimen: useful for infants when urine does not need to be sterile
o Catheterization: for any age incontinent patient where sterile urine specimen is needed
o Suprapubic aspiration: infants where genital anatomy makes cath difficult

41
Q

ESR

A

normal is 15-20mm/hr
increased in inflammatory d/o
affected by age, race, gender

42
Q

CRP

A
  • Produced in response to inflammatory cytokines (IL-1, IL-6, TNFalpha)
  • CRP activates the classic complement pathway
  • affected by gender, race
  • moderate elevation (1-10mg/dL) assoc. w/ rheumatoid diseases
43
Q

complement

A

o Measure levels of C3, C4, and CH50

o Useful in initial diagnosis of lupus (decreased complement in lupus)

44
Q

definition of rheumatoid factor

A

o Rheumatoid Factor (RF): IgM or IgG antibody against Fc portion of IgG.

45
Q

definition of Anti-CCP antibodies

A

• Recognize post-translational modification or arginine to citrulline (by peptidyl arginine deiminiase)
• Citrullinated vimentin, fibrin, collagen type II, filaggrin
-higher specificity than RF for diagnosis of RA

46
Q

ANA antibodies

A
  • Antibodies that bind nuclear factors (ds DNA, histones, RNA/Protein nuclear complexes)
  • Tested by IF (patterns include: homogenous, perinuclear, speckled, nucleolar)
  • Use serial dilution to estimate titer
  • High titer (must dilute pt’s serum a lot)—suggests high concentration or high affinity of autoantibody
  • Titer does not correlate with disease activity or prognosis
47
Q

anti-smith

A

(binds non-coding RNA complex) very specific for SLE, but only detected in 30% SLE pts

48
Q

anti-RNP

A

(binds non-coding RNA complex) found in pts with SLE, mixed connective tissue disorders

49
Q

anti-SSA

A

40% of patients with SLE, but also in primary or secondary sjogrens
• **placental transmission can cause neonatal lupus!

50
Q

anti-SSB

A

40% of patients with SLE and 15% patients with primary sjogrens

51
Q

anti-dsDNA

A

70% specific for SLE, titers used to assess SLE activity, correlate with development of SLE nephritis

52
Q

anti-centromere

A

limited scleroderma (CREST)

53
Q

Anti-Scl-70

A

very specific but not sensitive for systemic sclerosis/scleroderma

54
Q

anti-histone

A

drug induced lupus

55
Q

antiphospholipid antibodies

A
  • Anti-cardiolipin (IgG, IgM, IgA) and anti-B2 glycoprotein detected by ELISA
  • Lupus anti-coagulant: tests to detect inhibitor of phospholipid dependent clotting
  • Antibodies target cell membranes
  • Anti-phospholipid antibody syndrome: Pts present with coagulopathy, thrombocytopenia, recurrent fetal loss
56
Q

anti-Jo1

A

interstitial lung disease, raynaud’s, mechanic’s hands, polymyositis or dermatomyositis with moderate response to treatment

57
Q

anti-Mi2

A

dermatomyositis and good prognosis

58
Q

anti-SRP

A

: cardiac disease and severe weakness; good prognosis

Nephro (5 decks)

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