Renal Flashcards

1
Q

Fanconi syndrome: causes

A
Hereditary (Wilson's dz, glycogen storage dz)
Multiple myeloma
Ischemia
Lead tox
Drugs (expired tetracyclines, tenofovir)
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2
Q

Renal tubular defects

A

Fans Become Good and Loud Sometimes

Fanconi
Bartter
Gitelman
Liddle (Loud = gain of fxn)
SAME
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3
Q

Things excreted and by where in Fanconi syndrome

A

PCT defect
Don’t reabsorb: amino acids, glucose, HCO3, PO4

Fans Puke At Home Games

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4
Q

Acute interstitial nephritis:
Classic findings
P’s
Less common causes

A
Pyuria: EOSINOPHILS - no casts
Pee (diuretics)
Pain-free (NSAID's, Chronic ASA+Aceto)
PCN (and ceph)
PPI
rifamPin

Systemic infection, autoimmune (Sjogren, SLE, sarcoid)

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5
Q

Actue tubular necrosis causes

A

Ischemic (decreased renal blood flow)
Nephrotoxic (AG, contrast, crush injury)

Muddy brown casts

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6
Q

Renal papillary necrosis

A

SAAD papa

SCD
Acute pyelonephritis
Analgesics
Diabetes mellitus

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7
Q

Crescent formation pathophys

A

Macs and T cells pass into Bowman’s space
Fibrin leaks in via gaps in the membrane
Macs secrete factors than enhance deposition
Fibroblasts infiltrate and secrete collagen

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8
Q

Potter’s sequence:
Usual cause
Usual finding

A

Usually a renal cause that leads to decreased urinary output

Flat face, lower limb deformity, pulmonary hypoplasia, renal agenesis

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9
Q

Renal plasma flow =

A

PAH clearance

(urine PAH x flow rate) / plasma PAH

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10
Q

Renal blood flow =

A

PAH clearance / 1-hematocrit

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11
Q

Ammonia buffer system:
Stimulus
Starting amino acid
End result

A

Acidosis stimulates
Glutamine is broken down in tubule cell
Ammonia secreted into lumen and bicarb into blood

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12
Q

Do you replace catheters?

A

Nope! So stop picking that answer

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13
Q

Type of incontinence in MS

A

Urge incontinence

Spastic bladder

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14
Q

Spastic bladder vs. flaccid bladder

A

Spastic: hypertonia, frequency throughout day
Flaccid: increased residual volume, incontinence towards end of day

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15
Q

Transplant rejection path findings

A

Hyperacute (minutes/hours): preformed antibodies; cyanosis, arterial fibrinoid necrosis/thrombosis

Acute (<6mo): humoral (C4d depletion, neuts, nec vasculitis); cell mediated (lymphs)

Chronic (months-years): low grade immune response (suppresants); wall thickening, lumen narrowing, interstitial fibrosis, atrophy

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16
Q

You finally learned what the allantois is?

Three abnormalities, go:

A
Allantois = urachus in urogenital sinus
Remnant can lead to:
1. patent -> umbilical discharge
2. urachal sinus (failure to close distal) -> infection
3. cyst (middle persists)
17
Q

Repeat positive RPR assay -> next steps?

A

TP-EIA assay looking for trep. pal.

If neg -> SLE, especially anti-phospholipid-antibodies (prolonged PTT)

18
Q

Worst prognostic factor for PSGN?

A

Adult onset -> less likely to fully recover

19
Q

Where is the macula densa?
How about the JG cells?
Who secretes renin?

A

Macula densa -> distal tubule (sense hypoperfusion and stimulate JG cells)
JG cells -> in afferent arteriole (secrete renin)

20
Q

ADH upregulates what in the kidney?

A

TWO THINGS!

  1. Aquaporins in CT
  2. Urea in the medullary collecting duct
21
Q

Consequences of renal failure

A
MAD HUNGER
Met Acidosis
Dyslipidemia (inc. trigly)
Hyperkalemia
Uremia
Na+ retention
Growth retardation/developmental delay
EPO failure
Renal osteodystrophy (dec. vit D, inc. PTH, low Ca2+)
22
Q

Side effects of EPO therapy

A

Indicated with GFR<30
Thromboembolic events
HTN (via EPO receptors on vascular smooth muscle)

23
Q

Causes of anion ion gap metabolic acidosis

A

MUDPILES

Methanol
Uremia
DKA
Propolene glycol
INH, Infection
Lactic acidosis
Ethylene glycol
Saliycates
24
Q

Clear cell renal carcinoma histo findings

A

Big, clear cells

Glycogen and lipid accumulation in cells

25
Q

IgG4 and anti-phospholipase A2

A

1˚ membranous nephropathy

26
Q

Dietary risk for kidney stones

A
Low fluid
Low calcium
High oxalate
High protein
High sodium
High fructose
27
Q

Disease risk factors for kidney stones

A

1˚ hyperparathyroidism: high Ca
Cronhs: hyperoxaluria
Distal RTA: low citrate
Gout: high uric acid

High citrate in the urine prevents sontes

28
Q

Serum and urine findings (most commonly) with kidney stone

A

Hypercalciuria

Normocalcemia

29
Q

Most and least concentrated parts of a nephron

A

Most: bottom of loop
Least: top of PCT

30
Q

Aldosterone effects on CT and Na, K, HCO3 findings in primary aldosteronism

A

Na+ in (which negatively charges lumen)
Pulls K+ and H+ out -> met alk, hypoK
However, Na remains normal in 1˚ aldo

Na: nml
K+: low
HCO3: high