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Patho II, Renal > Glomerular and Tubular Diseases > Flashcards

Glomerular and Tubular Diseases Flashcards

1
Q

In 70kg person kidney filters about

A

180 L /d

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2
Q

What fraction of cardiac output goes to renal blood flow

A

20% - 25%

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3
Q

Classic collection of symptoms in glomerular

A

Hematuria
Proteinuria
Lowered GFR
HTN

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4
Q

Two different special constellations of symptoms that can manifest in patients with glomerulonephritis

A

Nephritic and Nephrotic syndromes

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5
Q

Nephrotic syndrome - collection of signs

A

Proteinuria (> 3.5g/day)

Hypoalbuminemia

Edema

Hyperlipidemia

Lipiduria

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6
Q

Nephritic syndrome - collection of signs

A

Accumulation of RBC, WBC, immune complexes, and some protein - forming casts, brown urine

Decreased GFR > High BP, Oliguria

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7
Q

Most common cause of secondary nephrotic syndrome

A

Diabetes

HTN #2

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8
Q

Five categories of glomerular disease

A

Acute glomerulonephritis
Rapidly progressive glomerulonephritis
Chronic glomerulonephritis
Nephrotic syndrome

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9
Q

The abrupt onset of hematuria and proteinuria with decreased GFR and salt/water retention. Typically followed by full renal recovery

A

Acute Glomerulonephritis

  • hypercellular / thickened glomerulus
    - narrowed capillaries
    - decreased filtration
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10
Q

Common cause of acute glomerulonephritis

A

Post-Strept, autoimmune

7-10 days after original infection

presents as Acute Nephritic Syndrome
(HTN, Hematuria, Increased BUN SrCr, Oliguria)

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11
Q

Most common cause of primary glomerulonephritis

A

Berger’s Disease

IgA nephropathy

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12
Q

Also called crescentric glomerulonephritis because of its tendency to cause proliferation of epithelial cells in the glomerulus.

Always autoimmune

Usually progresses to renal failure

A

Rapidly Progressive Glomerulonephritis

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13
Q

GFR trends in Rapidly Progressive Glomerulonephritis

A

GFR drops by 50% within 3 months

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14
Q

Rapidly Progressive Glomerulonephritis results when (specific to glomerulus)

A

When most of the glomeruli are damaged enough to allow FIBRIN to enter Bowman’s space, which prevents filtration and permanently scars

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15
Q

Wegener’s granulomatos is an example of what type of Rapidly Progressive Glomerulonephritis (RPGN)

A

Type III, ANCA antibodies

Antibodies not visible histologically

Makes up 50% of RPGN

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16
Q

SLE, IgA nephropathy, post-strep GN is an example of what type of RPGN

A

Type II, immune complex deposition

GRANULAR DEPOSITION OF COMPLEXES

25% of RPGN

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17
Q

Goodpasture’s is an example of what type of RPGN

A

Type I, Anti-GBM (antibodies to type IV collagen)

LINEAR DEPOSITION OF COMPLEXES

25% of RPGN

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18
Q

Patients with acute glomerulonephritis who develop chronic renal failure slowly over 5-20 years

A

Chronic Glomerulonephritis

19
Q

Typical features of chronic glomerulonephritis

A

Hypercellularity in the mesangium and obliteration of glomerular capillaries

Often found incidentally, occult proteinuria / HTN

*Significant scar tissue from ongoing autoimmune injury

20
Q

Hypercellularity in the mesangium and obliteration of glomerular capillaries are typical features of -

A

Chronic glomerulonephritis

21
Q

A classic example of chronic glomerulonephritis, and one of the most common causes of NEPHROTIC syndrome in adults

A

Membranous Glomerulonephritis

Autoimmune

25% recover completely

22
Q

Membranous GN vs RPGN Type II

A

Type II RPGN, immune complex deposition (IgA, SLE)

Unlike RPGN, in Membranus GN immune complexes trigger complement and MAC ATTACK

23
Q

Sudden appearance of proteinuria and edema (nephrotic), with unknown etiology. Relatively benign

A

Minimal Change GN

24
Q

Most common cause of renal failure

A

Secondary GM (diabetes, HTN, atherosclerosis, vasculitis)

25
Q

How to distinguish glomerular disease from interstitial or tubular

A

Patient Hx

UA

  • Hematuria
  • RBC Casts
  • Lipiduria
  • Proteinuria
26
Q

UA with red cells, casts, mild proteinuria.

More severe symptoms not present (edema, proteinuria >3.5g, HTN)

Patients often present with asymptomatic haematuria and proteinuria discovered on routine examination, or in IgA nephropathy for eg with episodes of gross haematuria

A

Focal Nephritic UA patterns

Damage to < 1/2 of patient’s glomeruli

27
Q

Similar to focal disease, but may also have heavy proteinuria (even nephrotic range), obvious edema, hypertension and/or renal insufficiency

‘full house’ urinary sediment – red cells, white cells, red cell casts, white cell casts, hyaline casts

A

Diffuse Nephritic UA patterns

Damage to all or nearly all glomeruli

28
Q

Heavy proteinuria (> 3.5g / d)

Lipiduria (Maltese cross)

Few cells, few casts

A

Nephrotic UA patterns

29
Q

Extrinsic causes of obstructive uropathy

A

Pregnancy

Inflammation (PID, peritonitis, diverticulitis, salpingitis)

Tumurs (PROSTATE, rectum, bladder, ovaries)

30
Q

Timeline of obstructive damage

A
  1. Collecting system dilates - triggers growth of new tissue in ureters
  2. Collecting system stretches and enlarges, damaging tubular cells
  3. Fibrosis begins in the tubules and the interstitial space (repair process)
  4. Fibrosis triggers cytokines, which causes more damage

1 week - 3 months

31
Q

Obstructive Uropathy Lab Findings

A

Dilute Urine (inability to concentrate)

Metabolic Acidosis (inability to secrete H+)

Hyperkalemia (inability to secrete K)

Hyponatremia (inability to reabsorb Na)

Uremia (can’t secrete urea)

32
Q

Common cause of AKI, usually occurs due to ischemia or drug exposure, usually diagnosed with elevated BUN/Cr levels

A

Acute Tubular Necrosis

Ischemic, Nephrotoxic

33
Q

Ischemic Acute Tubular Necrosis leads to

A

Tubule cell death > tubular occlusion by sloughed cell debris

> Tubule occlusion raises pressure at Bowman’s Space and LOWERS GFR

34
Q

Common Sites of Injury in Obstructive Uropathy

A

Uterosacral Ligament

Pelvic Brim

Crossing of Uterine Artery

Tunnel of Wertheim

Near Utero-vesicle junction

35
Q

How might ATN show in UA

A

Granular casts, muddy silty urine

36
Q

Sequence of ATN

A
  1. Initiation phase - drop in GFR, bump in BUN/Cr
  2. Maintenance phase - GFR low, BUNCr slowly rise, oliguria, uremia, fluid retention
  3. Recovery phase - tubular cells regenerate and function slowly recovers
37
Q

ATN phase in which there is a drop in GFR, bump in BUN/Cr

A

Initiation phase

38
Q

ATN phase in which GFR is low, BUNCr slowly rise, oliguria, uremia, fluid retention

A

Maintenance phase

39
Q

ATN phase in which tubular cells regenerate and function slowly recovers

A

Recovery phase

40
Q

Diseases associated with Nephrotic Syndrome

A

Primary Renal Disease

  • Minimal Change GN
  • Focal segmental glomerulosclerosis
  • Membranous GN

Secondary Renal Disease

  • SLE
  • Hep B C
  • HIV
  • DM
  • Malignancy
41
Q

Which kind of renal cystic disease can become neoplastic?

A

Acquired Renal Cystic Disease

  • usually a result of end stage renal disease
  • cysts found throughout, usually in cortex
42
Q

Autosomal Dominant PKD, which chromosome

A

Chromosome 16

Associated cysts throughout body

43
Q

Renal tumor found in infants/children

A

Wilm’s tumor / Nephroblastoma

44
Q

Renal cancer found in adults

A

Renal Cell Carcinoma, Adenoma, Oncocytoma

Patho II, Renal (2 decks)

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