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Genitourinary > Intrinsic Renal Failure (exam2) > Flashcards

Intrinsic Renal Failure (exam2) Flashcards

1
Q

Intrinsic causes of Renal Failure are up to what percentage

A

50%

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2
Q

The sites of damage for Intrinsic Renal Failure

A

Glomeruli, the interstitium, and or tubules

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3
Q

Most common cause of Intrinsic Renal Failure

A

Acute Tubular Necrosis (ATN)

-disease is secondary to ischemia or nephrotoxins

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4
Q

Nephrotic / Nephritic

A

Nephrotic think lots of protein loss. With Nephritic think lots of blood loss. So with nephritic think more of an inflammation process

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5
Q

ATN the BUN:Cr ratio is usually what

A

<20:1

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6
Q

what is ATN

A

Acute tubular necrosis

  • Acute damage to tubule epithelium of nephron
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7
Q

What percentage of Intrinsic AKI is from ATN

A

85% of cases

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8
Q

Two main causes of ATN

A

Ischemia & Nephrotoxin Exposure

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9
Q

GFR is increased or decreased in Ischemic Tubular injury

A

Decreased

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10
Q

How does Pre-Renal evolve into Intrinsic AKI

A

Because of Decreased or inadequate renal blood flow leading to hypoxic kidney cells and death of cells

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11
Q

Third leading cause of inpt Toxic tubular injuy comes from?

A

Radiologic contrast dye

Iatrogenic - happened by medical providers

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12
Q

Endogenous causes of toxic Tubular injury

A

Heme-containing proteins (myoglobin, hemoglobin)

heme- containing proteins, bence jones proteins, gout… etc.

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13
Q

Clinical presentation of ATN

A

Generally nonspecific signs and symptoms of Acute Renal Failure

They can include

  • Anorexia
  • Nausea/Vomiting
  • Delirium
  • weakness/fatigue
  • HTN
  • Coma/ seizures.
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14
Q

Diagnostic evaluation of ATN

A
  • Elevated BUN and Creatinine, Decreased GFT
  • usually BUN:Cr rat.- <20:1
  • Muddy brown sediment visible granular casts in Microscopic evaluation of Urinalysis
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15
Q

What electrolyte imbalances are often present with pts suffering from ATN

A

Hyperkalemia and Hyperphosphatemia

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16
Q

Urinary output of ATN

A

Variable

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17
Q

Renal absorption of sodium is often _______ . with ATN

A

impaired
- this results in and increased FEna - greater than or equal to 2%

increased sodium in urine

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18
Q

Tx of ATN

A

Remove the offending agent (if applicable)

Avoid volume overloading

Diuretics (if fluid overload)

Dialysis- may be included if life-threatening electrolyte abnormality.

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19
Q

Average maintenance phase of ATN is

A

1-3 wks

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20
Q

True or false - A nephrologists must be involved in all cases with ATN

A

True

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21
Q

What is Acute interstitial Nephritis

A

An inflammatory disorder of renal interstitium

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22
Q

What is the cause of Acute Iterstitial Nephritis in over 70% of cases

A

Drugs

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23
Q

Most common drugs that cause Acute Interstitial Nephritis

A

Penicillins, Cephalosporins, Sulfonamides, NSAID’s, PPIs, Rifampin, Phenytoin, and Allopurinol

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24
Q

Clinical presentations of Acute interstitial Nephritis

A

classic picture is that of a previously healthy pt developing suden renal dysfunction after starting a new medication (sometimes starting the new drug can cause a delay

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25
Q

Common Clinical presentation of Acute Interstitial Nephritsi

A

Fever- (80$)
Transient maculopapular rash(25-50%)
Flank pain d/t renal capsule distension
Myalgias and Arthralgias

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26
Q

Acute Interstitial Nephritis

Diagnostic EValuation

A

Elevated BUN and Creatinine
Decreased GFR
hematuria is common
Modest proteinuria

WBC’s present in urine in >95% of cases
WBC casts
CBC shows eosinophilia

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27
Q

True or false- renal imaging is helpful for Acute Interstitial Nephritis

A

False- not helpful

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28
Q

Renal Biopsy is or is not required for a definitirve diagnosis of Acute interstitial nephritis

A

Is =)

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29
Q

Treatment of Acute Interstitial Nephritis

A

Discontinue offending medication

Supportive care

1/3 pts require temporary dialysis

Corticosteroids

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30
Q

Most pts recover from acute interstitial Nephritis within?

A

a few weeks to months

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31
Q

Glomerulonephritis (GN) is comprised of what process

A

An inflammatory process involving primarily the glomerulus

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32
Q

what other structures can be effected by Glomerulonephritis

A

Renal vasculature
interstitium
tubular epithelium

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33
Q

Glomerulonephritis is relatively an uncommon cause of AKI corresponding to what percentage?

A

about 5%

34
Q

What damage can occur due to Glomerular inflammation

A

Damage to the glomerular basement membrane or capillary endothelium

35
Q

What is often the causation of the inflammatory process of Glomerulonephritis

A

Antigen-antibody complex formation and deposition

36
Q

Where do complexes or antibodies become trapped to cause the inflammation during the filtration with GN

A

the glomerulus

37
Q

what increases the risk / poorer prognosis with GN

A

The more glomeruli that are involved

38
Q

Infection-related GN

A

Sequela of group A beta-hemolytic Strep or Staph Aureus infection

39
Q

Clinical presentation of infection-related GN

A

Tea colored urine
Edema (common around mouth)
Oliguria
HTN

40
Q

What titer may be elevated for weeks in Infection-related GN

A

Antistreptolysin O (ASO)

41
Q

Most kids will recover spontaneously, or will not recover from Infection-related GN

A

recover spontaneously

42
Q

What percentage of Adults never fully recover from Infection-Related GN

A

30-70% of affected adults

43
Q

What is the other name for IgA Nephropathy

A

Berger’s Disease

44
Q

Pathophys of IgA Nephropathy

A

Deposition of IgA immune complexes in the glomeruli, causing structural damage

45
Q

What is the initial presentation of IgA Nephropathy

A

episode of hematuria

46
Q

Hallmark of Burger’s Disase

A

2-6 days of Hematuria

47
Q

Confirmation of IgA Nephropathy

A

Renal Biopsy

  • IgA deposition on immunohistology
48
Q

Tx of Burger’s

A

Teat the HTN with ACE or ARB

49
Q

What percentage of Burger’s disease suffering pts will have recurrent episodes

A

50%

-typically this leads to progressive, chronic loss of renal function and CKD

50
Q

What is HSP

A

Henoch-Schonlein Purpura

51
Q

Hsp is not only kidney disease but…

A

An acute systemic immune-mediated small vessel vasculitis

52
Q

What is the population that HSP effects mostly

A

Children less than 10 years of age

53
Q

Clinical presentation and course of Henoch-Schonlein Purpura

A

Children present with hematuria, and large purple purpura on lower extremities

Arthralgias, abd pain, and proteinuria

Generally self-limited resolving in 94% of pts within 4 weeks

54
Q

Membranoproliferative GN is due to

A

deposition of immune-complex and or complement factors

55
Q

What are the effects of Membranoproliferative GN

A

Mesangial cell proliferation and capillary wall remodeling

56
Q

Common population of Membranoproliferative GN

A

Children and young adults

57
Q

Clinical presentation of Membranoproliferative GN

A

Most commonly presents as nephrotic syndrome

May present with recurrent gross hematuria

58
Q

Diagnosis of Membranoproliferative GN requires what

A

Renal Biopsy

59
Q

TX of Membranoproliferative GN

A

Corticosteroids and cyclophosphamide

60
Q

if pts develop antibodies against the glomerular basement membrane (GBM) they have what disease

A

Anti-GBM Antibody Disease

61
Q

because of tissue similarity in capillaries in the lung Anti-GBM antibodies may also do what

A

affect the Lungs and cause Hemorrhage

62
Q

The anti-GBM antibody disease GN has also been known as what

A

Goodpasture’s syndrome

63
Q

Pts with Anti-GBM antibody disease GN can present how

A

with glomerulonephritis alone or with glomerulonephritis and hemoptysis together

64
Q

Diagnosis of anti-GBM GN

A

Made with anti-GBM antibodies testing

65
Q

TX for Anti-GBM GN

A

Plasma exchange, chemotherapy drugs, steroids

66
Q

Lupus Nephritis GN is secondary to what disease

A

Systemic Lupus Erythematosus (SLE)

67
Q

what percentage of Lupus pts suffer from Lupus Nephritis GN

A

about 50%

68
Q

What is the pathogenisis of Lupus Nephritis

A

Antinuclear antibodies (ANA) form immune complexes and cause inflammation and glomerular damage

69
Q

Diagnostic Criteria of Lupus Nephritis

A

Lupus, plus one or more of the following

Persistent proteinuria
Cellular casts
RBCs and or WBCs consistently in urine

70
Q

Indication of Renal biopsy is appropriate in all Lupus pts with evidence of nephritis

A

True

71
Q

Tx of Lupus Nephritis depends on the severity of the disease but can include

A

High-dose corticosteroids which often are used to treat the autoimmune condition.

ACE or ARB should be started as well

72
Q

Rapidly Progressing GN’s Clinical presentation

A

can be any of the glomerular conditions: not specific disease process.

73
Q

What is the range that loss of renal function occurs in Rapidly Progressing GN

A

Days to weeks

74
Q

Pts might have presentation of what in Rapidly progressing GN

A

Edema
Proteinuria
Hypertension
RBC casts

75
Q

What is Characteristic of RPGN

A

Crescent Formations on Renal Biopsy

76
Q

RPGN is represented by what percentage of GN

A

roughly 20 percent

77
Q

what is the Diagnostic Evaluation for a Glomerulonephritis (GN)

A
  • Serum Creatinine can rise over days to months
  • UA showing hematuria and proteinuria
  • UA microscopy will show cellular elements, such as RBCs, RBC casts and occasional WBCs
78
Q

What are characteristic of GN

A

RBCs and RBC casts

79
Q

Treatment of GN

A

Depends on underlying condition causing glomerulonephritis the treatment may consist of

  • High dose steroids
  • Cytotoxic Agents like cyclophosphamide
  • Plamsa Exchange (Goodpasture’s )
80
Q

True or False - Although complex Glomerulonephritis does not need a Nephrologist involved with every pt case immediately

A

False- because of the complexity Nephrologists should be involved immediately. PC PA’s should not attempt to manage these cases on their own .

Genitourinary (11 decks)

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