Renal Flashcards

1
Q

Goodpasture Synrdome - IF appearance?

A

Linear

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2
Q

Goodpasture Synrdome - Presentation?

A

Hematuria & Hemoptysis

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3
Q

Acute Poststreptococcal Glomerulonephritis - IF appearance?

A

Granular

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4
Q

Diffuse Proliferating Glomerulonephritis - IF appearance?

A

Granular

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5
Q

Characteristics of Nephritic Syndrome?

A
  • Inflammatory process
  • Hematuria & RBC casts
  • Azotemia, Oliguria, Hypertension
  • Proteinuria (<3.5 g/day)
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6
Q

Characteristics of Nephrotic Syndrome?

A
  • Massive proteinuria (>3.5 g/day, frothy urine)
  • Hyperlipidemia, fatty casts, edema

Ass’d w/ :

  • Thromboembolism/hypercoagulable state
  • ↑ risk of infection (loss of immunoglobulins)
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7
Q

Dx?

  • “Spike & Dome” appearance w/ subepithelial deposits on EM
  • Diffuse capillary & GBM thickening on LM
A

Membranous nephropathy

  • IF = Granular
  • SLE’s nephrotic presentation
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8
Q

What is SLE’s nephrotic presentation?

A

Membranous nephropathy

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9
Q

Membranous Nephropathy - IF appearance?

A

Granular

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10
Q

Dx?
LM = Normal glomeruli
EM = Foot process effacement

A

Minimal change disease
(Nephrotic)

  • Selective loss of albumin, not immunoglobulins
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11
Q

Most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis

2nd most common is membranous nephropathy

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12
Q

Dx?
LM = segmental sclerosis & hyalinosis
EM = effacement of foot processes

A

Focal segmental glomerulosclerosis

Nephrotic

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13
Q

Dx?

Congo red stain shows apple-green birefringence under polarized light

A

Amyloidosis
(Nephrotic)

  • ass’d w/ chronic conditions
    (e. g. multiple myeloma, TB, RA)
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14
Q

Dx?

  • Subendothelial IC deposits w/ granular IF
  • “Tram track” appearance
A

Membranoproliferative Glomerulonephritis
(Nephrotic)

  • “Tram track” appearance due to GBM splitting caused by mesangial ingrowth
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15
Q

Diabetic Glomerulonephropathy can cause non-enzymatic glycosylation of GBM & ______ arterioles.

A

efferent

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16
Q

Dx?

LM = Glomeruli enlarged & hypercellular, neutrophils, "lumpy bumpy" appearance
EM = Subepithelial immune complex humps
A

Acute Poststreptococcal Glomerulonephritis

17
Q

Dx?

Most frequently seen in children. Presents w/ peripheral & periorbital edema, dark urine, & hypertension. Resolves spontaneously.

A

Acute Poststreptococcal Glomerulonephritis

“sore throat (1 wk ago), face bloat, piss coke”

18
Q

Acute Poststreptococcal Glomerulonephritis - IF appearance?

A

Granular

  • due to IgG, IgM, & C3 deposition along GBM & mesangium
19
Q

Dx?

LM & IF = Crescent-moon shape

A

Rapidly progressive glomerulonephritis (RPGN)
(really just a description, not a separate disease)

  • Crescents consist of Fibrin & Macrophages
  • Potengial outcome of various renal pathologies in adults
20
Q

What is SLE’s nephritic presentation?

A

Diffuse Proliferative Glomerulonephritis

due to SLE or MPGN

21
Q

Dx?

LM = "wire looping" of capillaries
EM = subendothelial & sometimes intramembranous IgG-based ICs often w/ C3 deposition
A

Diffuse Proliferative Glomerulonephritis
(Nephritic)

IF = granular

22
Q

What is the most common cause of death in SLE?

A

Diffuse Proliferative Glomerulonephritis

23
Q

Nephritic syndrome related to Henoch-Schonlein purpura?

A

Berger’s Disease (IgA Nephropathy)

LM = Mesangial proliferation
EM = Mesangial IC deposits
IF = IgA-based IC deposits in mesangium
24
Q

Dx?

LM = Mesangial proliferation
EM = Mesangial IC deposits
- Often presents/flares w/ a URI or acute gastroenteritis

A

Berger’s disease (IgA nephropathy)

follows mucosal infection b/c of ↑IgA to fight off infection

25
Q

Dx?

  • Mutation in type IV collagen → split basement membrane
  • X-linked
A

Alport Syndrome

  • Glomerulonephritis, deafness
  • Eye problems (less commonly)
26
Q

PTH actions on renal tubules?

A

Early Proximal Tubule:
- Inhibits Na+/phosphate co-transport → phosphate excretion

Early Distal Convoluted Tubule:
- ↑Ca(2+)/Na+ exchange → Calcium absorption

27
Q

Amiloride - MOA?

A

Blocks Sodium absorption in Principals cells of Collecting tubules

28
Q

Triamterene - MOA?

A

Blocks Sodium absorption in Principals cells of Collecting tubules

29
Q

Thiazide Diuretics - MOA?

A

Block Na/Cl co-transporters in Distal Convoluted Tubule

30
Q

Loop Diuretics - MOA?

A

Block Na/K/2Cl co-transporters in Thick Ascending Limb (Loop of Henle)

31
Q

Angiotensin II actions on renal tubules?

A

Stimulates Na/H exchange in Proximal Tubules

→ ↑Na+, H2O, HCO3- reabsorption

32
Q

Causes: ↑anion gap metabolic acidosis

A

Methanol (formic acid), Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets, INH, Lactic acidosis, Ethylene glycol (oxalic acid), Salicylates (late)

“MUDPIILES”

33
Q

Causes: ↓anion gap metabolic acidosis

A

Hyperalimentation (↑Cl-), Addison’s disease (↓aldosterone), Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion (dilutes bicarbonate)

“HARD-ASS”

34
Q

What does the presence of casts indicate?

A

That hematuria/pyuria is of renal (vs. bladder) origin