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Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What is the definition of acute renal failure?

A

rapid onset of azotemia (increase BUN and Cr) and oliguria <500mL urine per day

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2
Q

what causes prerenal ARF?

A

hypoperfusion 2/2

vol depletion, heart failure, liver failure, sepsis, burns or bilateral RAS

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3
Q

what causes post renal ARF?

A

OBSTRUCTION
BPH
bladder or pelvic tumors
calculi

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4
Q

what causes intrinsic renal failure?

A

ATN
Allergic interstitial nephritis
glomerulonephritis
nephrotoxin exposure (including myoglobin from rhabdo)
renal ischemia (prolonged prerenal state that progresses to ischemia)

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5
Q

what are signs and symptoms of ARF?

A

oliguria
AGMA
hyperkalemia
arrhythmias

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6
Q

Urinary eosinophils suggest __________

A

allergic nephritis

athero-embolic dz

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7
Q

RBC casts are pathognomonic for ?

A

glomerulonephritis

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8
Q

muddy brown casts suggest ___________

A

ATN

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9
Q

how treat acute renal failure?

A
  • fluids to maintain urine output
  • diuretics to prevent volume overload
  • monitor electrolytes
  • Dialysis if recalcitrant vol overload, electrolyte abnormalities that are critical, unresponsive metabolic acidosis, toxic ingestion, uremia
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10
Q

What can we use in place of FENa if pt is on diuretics?

A

FE urea

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11
Q

Urine osms in prerenal vs. renal/postrenal

A

> 500 because urine is concentrated because body wants to hold onto water

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12
Q

What causes ATN?

A 
persistent prerenal states
rhabdo--> myoglobinuria
direct toxins (ampho, aminoglycosides, contrast dye)
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13
Q

what are the 3 phases of ATN

A

prodromal, oliguric and post-oliguric

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14
Q

how treat ATN?

A

treat precipitating cause
IVF to maintain UOP
monitor lytes
diurese PRN to prevent fluid overload

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15
Q

What can cause drug induced AIN?

A

b-lactams
sulfonamides
diuretics
NSAIDs

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16
Q

Si/Sx AIN?

A 
pyuria
maculopapular rash
eosinophilia
proteinuria
hematuria
oliguria
flank pain
fever
eosinophilia
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17
Q

Dx AIN

A

clinical improvement following withdrawal of offending drug

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18
Q

Tx AIN

A

removal of underlying cause, consider corticosteroids for allergic dz

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19
Q

Type 1 RTA characteristics? pH?

A

distal tubule defect of urinary H+ gradient
ph >5.5
when? ampho toxicity

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20
Q

Type 2 RTA characteristics? pH?

A

prox tubule failure to resorb HCO3
cause? acetazolamide, nephrotic syndrome, mult myeloma, Fanconi’s syndrome
pH >5.5 early then

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21
Q

Type 4 RTA characteristics? pH?

A

decreased aldosterone–> hyperkalemia and hyperchloremia
usually due to decreased secretion
when? diabetics, interstitial nephritis, NSAID/ACE or Heparin use

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22
Q

DI sx

A

polyuria, polydipsia, nocturia, urine spec grav 300

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23
Q

causes of central DI

A

1o -idiopathic

2o - trauma/infection/granulomatous infxn /fungal /TB infxn of pituitary

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24
Q

Tx central DI

A

desmopressin DDAVP (ADH analogue nasal spray)

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25
Q

Nephrogenic DI causes

A

1o - X linked

2o usually due to drugs: lithium, demeclocycline, rarely sickle cell, amyloid, multiple myeloma

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26
Q

Tx nephrogenic DI

A

increase water intake, sodium restrict

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27
Q

How differentiate central vs. nephrogenic DI?

A

hold water, administer vasopressin. in central DI, Uosm after deprivation isn’t greater than Sosm, but increases 10% after vasopression. (won’t change in nephrogenic)

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28
Q

Causes of SIADH

A

CNS dz: trauma, tumor, GBS, hydrocephalus
Pulm Dz: pneumonia, SCLC, abscess, COPD
Endocrine: hypothyroid, COnn
Drugs: NSAIDs, antidepressants, chemotherapy, diuretics, phenothiazine, oral hypoglycemics
PAIN

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29
Q

How Dx SIADH

A

hyponatremia with Uosm >300 and clinically NOT hypovolemic

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30
Q

How tx SIADH

A

evolemic: water restrict
- -> 3% saline or conivaptan if no response

hypovolemic: nml saline
* *beware of central pontine myelinolysis w/rapid correction of hyponatremia

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31
Q

What is chronic renal failure always associated with?

A

Azotemia of renal origin

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32
Q

What is Uremia?

A

clinical and biochem syndrome:

  • Azotemia
  • Acidosis (accumulate sulfates, phosphates, organic acids)
  • Hyperkalemia bc cannot excrete K+ in urine
  • Fluid volume disorder
  • Hypocalcemia due to lack of Vit D production
  • Anemia due to lack of Epo production
  • HTN 2/2 RAASq
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33
Q

Sx of uremia?

A 
anorexia
N/V
dementia
convulsions
coma
bleeding due to platelet dysfunction
fibrinous pericarditis--> tamponade
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34
Q

How Dx chronic renal failure?

A

reanl US–> small kidneys in chronic dz, anemia, diffuse osteopenia (bc decrease vit D since kidneys can’t convert it leads to decreased Ca absorption which causes increased PTH which leeches Ca from bones)

35
Q

Tx chronic renal failure?

A

salt and water restrict
diuresis to prevent fluid overload
dialysis to correct acid-base or severe electrolye disorders

36
Q

Sx nephrotic syndrome

A 
proteinuria >3.5g/day
edema
lipiduria with hyperlipidemia
marked decrease in serum albumin
hypercoagulation (due to loss of antithrombin III in urine)
37
Q

Minimal change dz:
WHO
Path
Tx

A

WHO: young kids, Hodgkins
PATH: EM shows fusion of podocyte foot processes
Tx: Prednisone

38
Q

FSGS
Who?
Assoc?
Tx

A

MCC hispanics and African American’s
clinically similar to MCD, but occurs in adults with refractory HTN
-usually idiopathic, can be assoc with HIV, heroin, diabetes, sickle cell
idiopathic type: young hypertensive males
Light micro: focal because only affects some glomeruli, segmental because only affects part of the glomerulus
Tx: prednisone and cyclophosphamide
poor prognosis–> chronic renal failure

39
Q

Membranous Glomerulonephritis
Who
Cause
Tx

A

MCC in caucasian adults
-slowly progressive disorder with decreased response to treatment seen
Causes
-infxn: HBV/HCV/Syph/Malaria
-drugs: gold salts, penicillamine in RA pts
-occult malignancy
-SLF
TX = prednisone and cyclophosphamide, 50% pts–> ESRD
**due to immune complex deposition

40
Q

Membranoproliferative glomerulonephritis
Types
Tx

A

*thick capillary membrane on H+E with tram track appearance
due to immune complex deposition
mesangial cell has proliferative cytoplasm
TYPE 1: subendothelial deposits, slowly progressive
TYPE 2: more aggressive, assoc with C3 nephritic factor–> overactive complement, decreased serum C3
TX: pred _ plasmapheresis or inferferon a, very poor prognosis

41
Q

how dx nephrotic glomerulopathies?

A

bx

42
Q

What is the general treatment for nephrotic syndrome

A 
protein restriction
salt restriction
diuretic
tx for edema
statin for hyperlipidemia
43
Q

What are the main causes of systemic glomerulopathies

A

diabetes
HIV
renal amyloidosis
Lupus

44
Q

What is the main manifestation of diabetes nephropathy? tx?

A

microalbuminuria
ACEi–decrease progression to renal failure
strict glycemic and hypertensive control
bx: Kimmelstiel Wilson nodules
as dz progresses only tx is renal transplant

45
Q

HIV nephropathy characteristics

A

usually seen in HIV acquired from drug use
–> FSGS
early antiretroviral tx may help kidney dz

46
Q

reanl amyloidosis dx and tx

A

dx: birefringence with congo red stain
tx: transplant bc dz recurs

47
Q

What are the main characteristics and tx for Lupus Nephropathy type 1

A

no renal involvement by histo

48
Q

What are the main characteristics and tx for Lupus Nephropathy type 2

A

mesangial dz with FSG pattern, no tx

49
Q

What are the main characteristics and tx for Lupus Nephropathy type 3

A

focal proliferative dz

tx: aggressive pred and cyclophosphamide

50
Q

What are the main characteristics and tx for Lupus Nephropathy type 4

A

diffuse proliferative dz, mos severe
nephrotic/nephritic presentation
LM–> wire loop abnormality
tx: pred+ cyclophos maybe transplant

51
Q

What are the main characteristics and tx for Lupus Nephropathy type 5

A

membranous dz

tx: pred

52
Q

what cuases nephritic syndrome

A

diffuse glomerular inflammation

53
Q

Sx of nephritic syndrome

A 
acute onset hematuria (smoky brown urine)
decreased GFR resulting in azotemia
oliguria
HTN
edema
54
Q

classic dyad in RAS?

A

sudden HTN with low K+ in a pt not on diuretics

55
Q

PSGN: presentation

A

s/p strep (or any infxn)
labs: RBCs and RBC casts in urine, azotemia, decreased C3, increased ASO titer
immunofluorescence–> coarse granular IgG or C3 deposits

56
Q

PSGN: tx

A

none, usually self limited

57
Q

Crescentic (rapidly progressive) glomerulonephritis

A

progresses to renal failure in weeks to months

58
Q

What is the main presentation and immunoflourescence pattern of goodpasture’s?

A

pres: 90% pres w/hemoptysis
+ anti GBM antibody
immunofluorescence–> smooth, linear deposition of IgG

59
Q

Tx of crescentic/goodpastures

A

prednisone and plasmapheresis

60
Q

Cause and sx of Berger’s dz

A

cause = IgA deposition in mesangium

sx: recurrent hematuria with low-grade proteinuria

61
Q

result of Berger’s dz

A

25% to renal failure

62
Q

tx of Berger’s

A

prednisone for acute flares, won’t halt dz progression

63
Q

Henoch schonlein purpura what IgG? who? pres?

A

IgA
Kids
ab pain, vomiting, hematuria and GI bleed often after respiratory infxn

64
Q

Henoch schonlein purpura tx

A

none, usually self limiting

65
Q

multiple myeloma kidney sx

A

tubular plugging 2/2 Bence jones (light chain) proteins
2o hypercalcemia
myeloma cells can directly invade kidney parenchyma

66
Q

what infxns are multiple myeloma patients susceptible to?

A

encapsulated organisms–> chronic renal failure

67
Q

causes of RAS?

A

atherosclerosis and fibromuscular dysplasia

68
Q

what is a screening for RAS?

A

oral captopril–> increase in renin

69
Q

how confirm RAS

A

angiography

70
Q

tx RAS

A

surgery vs. angioplasty

71
Q

MCC urinary tract obstruction in kids vs adults

A

kids: congenital
adults: BPH and stones

72
Q

50% of calcium pyrophosphate stones are assoiated with _______

A

idiopathic hypercalciuria

73
Q

ammonium magnesium aka struvite stones are radio_____

A

opaque (bc magnesium is heavy)

74
Q

ammonium magnesium aka struvite stones are usually due to which bugs

A

bugs that produce urease:
proteus
staph saphrophyticus
will cause pH to rise

75
Q

uric acid stones are radio____

A

lucent

76
Q

uric acid stones due to

A

gout

increased cell turnover (malignancy)

77
Q

tx uric acid stones

A

alkalinize urine, treat underlying disorder

78
Q

how does renal cell disseminate

A

hematogenously, invades renal vein and IVC

79
Q

sx renal cell cancer

A

hematuria, palpable mass, flank pain, fever, 2o polycythemia

80
Q

tx renal cell

A

resection
systemic IL-2
poor prognosis

81
Q

Wilms tumor: what age group? sx?

A

incidence peaks 2-4 years (vs. neuroblastoma, echymosis with proptosis, MC metastatic tumor in kids)
sx: palpable flank masses

82
Q

what syndrome can Wilms tumor be a part of?

A 
WAGR
W: Wilms
A: aniridia
G: genitourinary malformations
R: mental retardation
83
Q

tx wilms

A

nephrectomy plus chemo and radiation

Medicine (8 decks)

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