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FA17 Nephrology > GN 2 > Flashcards

GN 2 Flashcards

1
Q

nephrotic syndrome hallmark clinical findings

A

proteinuria >3g/day

peripheral edema

hypoalbuminuria

(may have just the proteinuria)

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2
Q

etiologies of nephrotic syndrome

A

1/3 = systemic disease with renal manifestations

2/3 = idiopathic

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3
Q

systemic diseases causing nephrotic syndrome

A

amyloidosis

diabetic nephropathy

HIV nephropathy

SLE

hep C

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4
Q

types of idiopathic nephrotic syndrome

A

minimal change dz
membranous nephropathy
focal segmental glomerulosclerosis

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5
Q

amyloidosis nephrotic syndrome

A

associated with multiple myeloma (AL) or RA, IBD, and chronic infection (AA)

misfolded non-fxnl proteins

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6
Q

diabetic nephropathy

A

MC in type I

DM pts are prone to other renal dz (papillary necrosis and nephritis)

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7
Q

nephrotic syndrome s/s (6)

A

peripheral edema

abdominal fullness

dyspnea

increased infection

hypercoagulability

protein calorie malnutrition

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8
Q

peripheral edema nephrotic syndrome

A

LOW serum albumin causes drop in oncotic pressure shift to 3rd space

this also causes abdominal fullness (ascites) and dyspnea

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9
Q

dyspnea nephrotic syndrome

A

due to pulmonary edema, pleural effusion, ascites on diaphragm

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10
Q

infection nephrotic syndrome

A

due to urinary loss of Ig and complement

also have increased susceptibility to pneumococcus

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11
Q

hypercoagulability

A

increased likelihood of arterial and venous thromboemoboli

particular FVT and renal vein thrombosis

renal vein thrombosis - be sure to distinguish from stone

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12
Q

protein calorie malnutrition

A

negative protein balance

more is being excreted than is being taken in

catabolic state may be masked by weight gain from edema

causes vitamin deficiencies (loss of binding proteins)

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13
Q

lab derangements off nephrotic syndrome

A

decreased serum albumin

hyperlipidemia

vitamin deficiencies

elevated ESR (increased fibrinogen)

hypocalcemia

U/A - proteinuria and oval fat bodies

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14
Q

hyperlipidemia nephrotic syndrome

A

hepatic production of lipids increases to maintain oncotic pressure despite losing so much protein in urine

decreased VLDL clearance

inflammation also exists - accelerated CAD

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15
Q

hypocalcemia why in nephrotic syndrome

A

vitamin D deficiency

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16
Q

tests used to elucidate etiology of nephrotic syndrome

A

ANA

C3/C4/complement

SPEP/UPEP

infectious dz work up

renal biopsy

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17
Q

general management of nephrotic syndrome

A

Diet and Edema control

hyperlipidemia management

anticoagulation

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18
Q

diet and edema nephrotic syndrome

A

SALT restriction

diuretics (loop and TZD will be higher doses)

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19
Q

hyperlipidemia management nephrotic syndrome

A

diet and exercise don’t help

aggressive pharmacotherapy

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20
Q

hypercoaguable state nephrotic syndrome

A

prone to membranous glomerulopathy and Afib

anticoagulant 3-6 months for thrombosis or until dz is controlled

consider prophylactic anticoagulation

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21
Q

minimal change dz (Nil Dz)

A

mc in children, can affect adults

adults: M=F, children: M>F

may be idiopathic, follow URI, or paraneoplastic syndrome (Hodgkin), associated with drugs (NSAID)

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22
Q

manifestations of Nil Dz

A

susceptible to infection

tendency to thromboembolic events

CAN cause acute renal failure

severe hyperlipidemia, protein malnutrition

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23
Q

Nil Dz renal biopsy

A

tissue looks almost completely normal

little disposition of immune complexes

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24
Q

minimal change disease tx

A

prednisone 1mg/kg/day
adults longer

some patients become resistant to corticosteroid

majority of patients will relapse and req steroid again - ESRD progression rare

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25
Q

membranous nephropathy etiology

A

common cause of nephrotic syndrome in adults (idiopathic)

in children usually secondary disorder

26
Q

membranous nephropathy disease

A

AutoAb against phospholipid receptor (PLA2-R) on podocyte of glomerulus

immune complex deposition in glomerular capillary walls and thickening of GBM

no hypercellularity on biopsy

27
Q

membranous nephropathy medication induced

A

medications for another disease cause issue

malignancies: Lung and GI
infections: HBV, endocarditis, syphilis
autoimmune dz: SLE, thyroiditis, mixed connective tissue
drug exposure: NSAID

28
Q

membranous nephropathy

A

typical symptoms and signs of nephrotic syndrome

AKI is rare

normal BP and normal GFR

29
Q

membranous nephropathy diagnosis

A

serologic assays for PLA2R Abs

does not req. renal biopsy

30
Q

disease conditions in membranous nephropathy

A

higher incidence of neoplasm - usual age appropriate screenings (Chest CT, colonoscopy, PSA, mammogram, pap/pelvic)

high risk of thromboembolic event

high risk of renal vein thrombosis

31
Q

treatment of membranous nephropathy

A

risk stratification based on 24 hr urine protein level and Cr clearance

Low: ACE/ARB, BP/hyperlipidemia to goal
Moderate/HR: same +immunosuppression

excellent for renal transplant

32
Q

treatment membranous nephropathy

low risk

A

proteinuria <3.5 g/day

low salt diet, strict BP control, ACE inhibitor

33
Q

treatment membranous nephropathy

moderate risk

A

3.5-8 g/day normal renal fxn

low salt diet, strict BP control, ACE inhibitor +/- immunosuppression

34
Q

treatment membranous nephropathy

high risk

A

8 g/day normal renal fxn

low salt diet, strict BP control, ACE inhibitor +immunosuppression

35
Q

Focal Segmental Glomeurlosclerosis (FSGS)

A

primary idiopathic/ secondary to DM, GIV, vesicurethral reflux

nephrotic syndrome + evidence nephritic symptoms (microscopic hematuria at diagnosis, HTN)

36
Q

FSGS renal biopsy

A

segmental areas of mesangial sclerosis

cloppase in some of glomeruli

37
Q

primary FSGS presents + Tx

A

rapid decline of renal function

more likely to have nephrotic syndrome

Tx: high dose steroids for 2-3 months, taper

38
Q

secondary FSGS presents + Tx

A

gradual decline in renal function over years

proteinuria may reach nephrotic levels, rarely develop nephrotic syndrome

supportive care + ACE inhibitors

39
Q

tubulointerstitial disease

A

disease of kidney outside glomerulus

acute or chronic

40
Q

acute tubulointerstitial disease (AIN)

A

hypersensitivity to medications

toxins/ischemia

interstitial edema, PMN infiltration, tubular cell necrosis

41
Q

drugs that often cause AIN

A

ABX (PCN, Cephalosporins, sulfa)

NSAIDs

Rifampin

PPI

42
Q

AIN patho

A

begins abruptly, AKI within days of exposure

subset of DRESS (drug rash with eosinophilia and systemic syndromes)

43
Q

NSAID AIN

A

BEGINS WEEK TO MONTHS AFTER USE

mc in elderly

nephrotic syndrome

44
Q

AIN presentation

A 
rash 
fever 
eosinophilia 
eosinophiluria 
elevated IgE (allergic)
45
Q

rifampin AIN

A

DOESN’T cause EOSINOPHILIA

usually occurs following reintroduction

DRSS

46
Q

other causes of AIN besides drugs

A

immunologic disease

acute renal transplant rejection

infections (any type of infection will cause)

47
Q

AIN treatment

A

promptly DC offending drug or treat underlying disease

document allergy

can hive high dose of steroid over 4-6 weeks

excellent supportive care

48
Q

chronic tubulointerstitial disease

A

acute insult or progressive insult without acute cause

interstitial fibrosis and atrophy are often seen

49
Q

main causes of chronic tubulointerstitial disease

A

obstructive uropathy
vesicoureteral reflux
analgesics
heavy metals

50
Q

obstructive uropathy

A

prolonged obstruction of urinary tract (BPH, stone, carcinoma, retroperitoneal tumor/fibrosis)

UO alternates bt polyuria and oliguria

HTN + azotemia

back flow of uric into kidney

51
Q

obstructive uropathy treatment

A

BPH and stones - usual tx

pelvic tumor: stent, tx underlying cause

52
Q

retroperitoneal fibrosis

A

rare, encases ureters and abdominal organs in fibrotic tissue

can be caused by meds, biologic agents, cancers

diagnose by CT + contrast, CT biopsy

secondary = tx underlying dz + steroid

primary = steroid, tamoxifen, immunosuppressive

53
Q

vesicoureteral reflux

A

urine passes retrograde during voiding due to incompetent vesicoureteral sphincter

disorder of child hood (typically renal damage before 5 y/o)

inflammatory response + fibrosis progressing to ESRD

54
Q

VUR epidemiology

A

caucasian, red head, male neonates, female mc children

55
Q

diagnosis of vesicoureteral reflux

A

voiding cystourethrogtaphy (VCUG)

recommended in children with UTI and siblings of persons with VUR

56
Q

VUR treatment

A

keeping patient infection free

significantly decrease risk of renal damage (prophylactic ABX and monitored)

young patents - conservative tx,

57
Q

analgesics chronic tubulointerstitial disease

A

ingestion of large quantities of analgesics for chronic pain (esp. combo pills)

MC in women

hematuria, mild proteinuria, polyuria, anemia, sterile pyuria

58
Q

analgesics chronic tubulointerstitial disease patho

A

kidney tries to excrete large quantities

become concentrated at papillary tip (10x that of serum)

cause inflammation and papillary tip necrosis - sloughing

59
Q

heavy metals that cause analgesics chronic tubulointerstitial disease

A

lead
cadmium
mercury
bismuth

accumulate and cause cell scaring, fibrosis

60
Q

other causes of chronic tubulointerstitial disease

A

Lithium

imunologic dz

neoplasia

atherosclerotic kidney dz

genetics

metabolic d

61
Q

general manifestations of chronic tubulointerstitial disease

A

polyuria due to inability to concentrate urine

may also have dehydration and salt wasting

hyperkalemia due to aldosterone restance

hyperCl due to renal tubular acidosis (decreased ammonia, inability to acidly, bicarb wasting)

62
Q

diagnosis of chronic tubulointerstitial disease

A

UA non specific - brand waxy casts + proteinuria

ID underlying disorder

quantify degree of fibrosis on biopsy

FA17 Nephrology (13 decks)

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