Renal Flashcards

1
Q

Minimal Change Disease

A

Primary Glomerular Disease, selective albumin loss (loss of anions of BM), Only visible on EM - foot process effacement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

EM spike and dome appearance with subepithelial deposites.

A

membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

second most common cause of primary nephrotic syndrome in adults

A

membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

nephrotic syndrome causes

A

focal segmental glomerulosclerosis, membranous nephropathy, minimal change disease (Lipoid nephrosis), amyloidosis, MPGN - membranoproliferative glomerulonephritis, diabetic glomerulonephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

frothy urine with greater than 3.5 g/day protein. hyperlipidemia, fatty casts, and edema.

A

nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

LM - diffuse capillary and GBM thickening

A

membranous nephropathy - drugs, infections, SLE and solid tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

focal vs diffuse glomerular problems

A

> or < 50% of glomeruli involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

nephritic syndromes

A

acute post-strep glomerulonephritis, rapidly progresive glomerulonephritis, Berger’s, Alport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

both nephritic and nephrotic

A

diffuse proliferative glomerulonephritis, Membranoproliferative glomerulonephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most common congenital renal anomaly.

A

horseshoe kidney - turner syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Potters sequence

A

flat face, low ears, limb abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of Potters

A

Oligohydramnios - bilateral renal agenesis, autosomal recessive PKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cysts in kidney, unilateral, surrounded by abnormal tissue (cartilage), non-inherited

A

dysplastic kidney - malformation of renal parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cysts in the kidneys, bilateral, cortical and medullary, infants, hepatic fibrosis (portal hypertension), hepatic cysts

A

autosomal recessive PKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

cysts in the kidneys, bilateral, cortical and medullary, young adults, berry aneurysms, hepatic cysts and mitral prolapse

A

autosomal dominant PKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

shrunken cystic kidneys, medullary collecting ducts, parenchymal fibrosis - worsening renal failure

A

medullary cystic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Azotemia

A

urea, creatinine, and other nitrogen rich compounds in the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

most common ARF

A

acute tubular necrosis - intrarenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Prerenal azotemia

A

bun/cr >15, FENa <1, normal urine concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

early postrenal azotemia

A

increased BUN/Cr, normal FENa and urine osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

late postrenal azotemia

A

decreased BUN/Cr, FENa >2, decreased urine osmolality <500

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

brown granular casts are seen in urine

A

Acute tubular necrosis, intrarenal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

intrarenal azotemia

A

decreased BUN/Cr, FENa >2, decreased urine osmolality <500

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

etiology of acute tubular necrosis

A

eschemic (proximal tubule, medullary TAL), nephrotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

nephrotoxic

A

aminoglycosides, heavy metals, myoglobin, ethylene glycol, radiocontrast dye, urate

26
Q

aminoglycosides

A

-mycins, gram (-) aerobes

27
Q

decrease rate of chemo urate induced ATN

A

hydration and allopurinol

28
Q

oliguria, rash, fever days to weeks after starting NSAIDs, Penicillin, or diuretics. eosinophils in urine

A

acute interstitial nephritis - may progress to renal papillary necrosis

29
Q

gross hematuria and flank pain - result of ; chronic phenacetin or aspirin, DM, Sickle Cell, or severe acute pyelonephritis.

A

renal papillary necrosis

30
Q

oxalate crystals in urine

A

ethylene glycol - nephrotoxic acute tubular necrosis

31
Q

Tumor lysis syndrome

A

initiating Chemo causes excessive waste in nitrogen products (urate) - nephrotoxic ATN

32
Q

avoid tumor lysis syndrome

A

hydration and allopurinol

33
Q

causes of acute interstitial nephritis

A

NSAIDs, penicillin, diuretics

34
Q

nephrotic syndrome in hispanic, african american, HIV, heroin, and sickle cell

A

focal segmental glomerulosclerosis - FSGS

35
Q

nephrotic syndrome in caucasian adults

A

membranous nephropathy

36
Q

glomerular subepithelial deposits

A

membranous nephropathy

37
Q

causes of subepithelial deposits

A

Hep B and C, solid tumors, SLE, drugs (NSAIDs, penicillamine)

38
Q

tram track appearance

A

type I membranoproliferative glomerulonephritis

39
Q

subendothelial deposits associated with HBV and HCV

A

type I membranoproliferative glomerulonephritis

40
Q

intramembranous deposits associated with C3 nephritic factor (autoantibody stabilizes C3 convertase)

A

type II membranoproliferative glomerulonephritis

41
Q

all glucose and amino acid resorption occurs in

A

PCT - as well as 65% of all other ions

42
Q

drives reabsorption in the PCT

A

Na/K pump

43
Q

AA and glucose pct resorption is coupled to

A

Na

44
Q

Type I vs II DM

A

lack of insulin or decreased sensitivity.

45
Q

post pituitary hormones

A

ADH/vasopressin and oxytocin

46
Q

descending loop of henle

A

20% reabsorption of filtered water

47
Q

paracellular absorption of Mg and Ca

A

ascending loop

48
Q

loop diuretics

A

furosemide, ethacrynic acid, bumetinide

49
Q

side effects of hyponatremia, hypokalemia, metabolic alkalosis

A

loop diuretics

50
Q

treat HTN and CHF. blocks NaCl symporter

A

hydrochlorothiazide

51
Q

blocks aldosterone receptors - blockade of Na/K and H/K exchange pumps

A

spironolactone

52
Q

side effects of spironolactone

A

hyperkalemic metabolic acidosis

53
Q

water absorption in cortical collecting ducts

A

vassopressin

54
Q

renal mass in 3 yo

A

Wilms tumor - nephroblastoma

55
Q

deletion in chromosome 11, histo collection of cells resembling primitive glomeruli.

A

wilms tumor - nonpainful, bilateral, good prognosis

56
Q

organomegaly, macroglossia, and neonatal hypoglycemia with wilms tumor

A

beckwith-weidemann syndrome

57
Q

abdominal mass in 2-4yo elevated catecholamines

A

neuroblastoma - neural crest cell derivative

58
Q

wilms benign or malignant

A

malignant

59
Q

child abdominal mass is most likely… mesodermal in origin

A

wilms tumor

60
Q

bence jones proteinuria

A

associated with multiple myeloma - of marrow