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Flashcards in Firecracker IV Deck (41)
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1
Q

First presenting symptom of Goodpasture syndrome

A

hemoptysis

2
Q

Second presenting symptom of Goodpasture syndrome

A

Hematuria

3
Q

Why do you get hemoptysis (and cough and SOB) in Goodpasture syndrome?

A

Pulmonary hemorrhage

4
Q

Why do you get hematuria in Goodpasture syndrome?

A

Rapidly progressive renal failure with S/Sx of nephritic syndrome

5
Q

Three presenting signs of pulmonary hemorrhage

A

hemoptysis, cough, dyspnea

6
Q

Presenting signs of RPGN

A

hematuria (2nd presenting symptom), RBC casts, azotemia, oliguria, mild/moderate hypertension, mild/moderate proteinuria and edema

7
Q

Timeline of Goodpasure

A

Hemoptysis –> couple weeks –> hematuria

8
Q

What are the deposits in IgA nephropathy

A

Mesangial deposition of IgA1, often with C3 and properdin

9
Q

Which Ig is produced by mucosal tissue & follows infections of mucosal tissue

A

IgA

10
Q

Adolescents/young adults with nephrotic syndrome and a nephritic component (eg, hematuria) → slow progression to renal failure

A

MPGN (membranoproliferative glomerulonephritis):

11
Q

MPGN type I and type II glomerular appearance

A

Glomeruli are large and hypercellular due to WBC infiltrate, proliferation of mesangial cells and endothelial cells, and ↑ mesangial matrix

12
Q

Mesangial ingrowth and new GBM (glomerular basement membrane) synthesis in response to deposition of immune complexes → duplication/splitting of GBM → thick GBM w/ “tram-track” or “double contour” appearance (esp. evident w/ silver or PAS stains)

A

MPGN types I and Ii

13
Q

location of IC in MPGN type 1

A

Subendothelial

14
Q

location of IC in MPGN type 2

A

membranoproliferative

15
Q

complement in MPGN type 1

A

Activates both classical and alternative complement → ↓ serum C1, C4, C3

16
Q

complement in MPGN type 2

A
  • Activates alternative complement only → ↓ serum C3; normal C1 and C4
  • Associated with C3 nephritic factor, an IgG autoantibody that stabilizes C3bBb (alternative complement C3 convertase) → persistent C3 activation → ↓ serum C3
17
Q

composition of ICs in MPGN type 1

A

Subendothelial immune complex deposits of C3, IgG, and early complement components C1, C4

18
Q

composition of ICs in MPGN type 2

A

Intramembranous immune complex deposits of C3 and IgG only

19
Q

AI causes of secondary MPGN (type 1)

A
  • SLE (systemic lupus erythematosus)

- SS (sjögren’s syndrome)

20
Q

Infection causes of secondary MPGN type 1

A
  • Hepatitis C, usually with cryoglobulinemia
  • Hepatitis B
  • HIV
  • Schistosomiasis
21
Q

malignancy causes of secondary MPGN type 1

A
  • CLL (chronic lymphocytic leukemia)

- Lymphoma

22
Q

besides panacinar emphysema, alpha1-antitrypsin deficiency causes

A

secondary MPGN type 1

23
Q

benign congenital disorder characterized by cystic dilations of medullary collecting ducts (“swiss cheese” appearance of medulla on intravenous pyelogram); renal cortex is spared

A

Medullary sponge kidney

24
Q

benign cysts usually located in the renal cortex of normal-sized kidneys.

A

Localized (simple) renal cysts

25
Q

multiple cysts in cortex and medulla associated with end-stage renal disease and chronic dialysis therapy

A

Acquired renal cystic disease

26
Q

Most patients are asymptomatic in medullary sponge kidney, but the most common symptoms/complications include:

A

1) Recurrent kidney stones (60% of cases)
2) Hematuria
3) UTI

27
Q

Most common type of asymptomatic renal mass

A

simple renal cysts

28
Q

most patients are asymptomatic with simple renal cysts, but what might still be found on urinanalysis

A

Microscopic hematuria is occasionally a benign, incidental finding on urinalysis.

29
Q

Patients on dialysis with acquired renal cystic disease have an increased risk of

A

renal cell carcinoma

30
Q
  1. Hereditary nephritis → hematuria, RBC casts
  2. Sensorineural hearing loss
  3. Ocular abnormalities
A

Alport syndrome

31
Q

types of ocular abnormalities seen in alport syndrome

A

(e.g., lens dislocation, posterior cataracts, corneal dystrophy)

32
Q

85% of cases of Alport syndrome are due to an X-linked recessive defect in the

A

α5 chain of type IV collagen

33
Q

Regardless of inheritance pattern or the specific defect involved, all cases of Alport syndrome are caused by

A

defective type IV collagen assembly

34
Q

defective type IV collagen assembly → structural-functional defects in the:

A
  • GBM
  • Cochlear hair cells of the inner ear
  • Lens and cornea of the eye
35
Q

Alport disease on EM

A

Irregular thickening/thinning of the GBM with splitting/lamination of the lamina densa → this often gives the GBM a unique “basketweave” appearance

36
Q

Kimmelstiel-Wilson

A

diabetes nephropathy

37
Q

nodular formation in diabetic nephropathy due to deposition of

A

type IV collagen (aka microangiopathy)

38
Q

Common causes of pre-renal azotemia that can progress to ischemic ATN include

A
hypovolemia, 
impaired cardiac function, 
hypoalbuminemia, 
renal artery stenosis, 
NSAID use
39
Q

ATN initiation phase is during the first 36 hours after the initial insult.

A

There is a slight decrease in urine output and an increase in BUN.

40
Q

The maintenance phase starts 36 hours after the initial insult in ATN

A

marked oliguria and increasing BUN.

41
Q

The recovery phase of ATN occurs when the tubule epithelium regenerates.

A

Diuresis is drastically increased, and BUN returns to baseline.