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GU > Lecture 2: AKI > Flashcards

Lecture 2: AKI Flashcards

1
Q

What characterizes AKI?

A
  • Decreased GFR
  • Increased BUN and/or creatinine
  • Decreased urine volume

Serum Cr takes time to elevate, so kidneys may be injured for longer.

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2
Q

What is the preferred criteria for AKI?

A

KDIGO

Staging of 1-3, requires serum Cr and urine output.

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3
Q

In what demographic is AKI most common in?

A

ICU patients.

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4
Q

What is the 24-hour urine output for anuria, oliguria, and polyuria?

A
  • Anuria: < 50mL/24hrs
  • Oliguria: < 400 mL/24hrs
  • Polyuria: > 2500 mL/24hrs.
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5
Q

Define azotemia.

A

Increased nitrogenous waste in blood.

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6
Q

Define uremia.

A

Symptoms caused by azotemia.

Azotemia can be asymptomatic.

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7
Q

What are the 3 types of AKI?

A
  • Prerenal (blood flow)
  • Intrarenal
  • Postrenal (Ureter)

Postrenal is the rarest AKI type.

However, it is possible to have multiple types of AKI concurrently.

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8
Q

What is the most common type of AKI and its underlying etiology?

A

Prerenal azotemia caused by renal hypoperfusion.

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9
Q

What are the 3 primary etiologies that result in renal hypoperfusion?

A
  • Hypovolemia
  • Decreased CO
  • Altered SVR
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10
Q

What BUN:Cr, urinary sodium, and urine osmolality tend to reflect prerenal azotemia?

A
  • BUN:Cr > 20:1
  • Urinary sodium = low
  • Urine osmolality = normal/elevated

Urea absorption is because the kidneys are attempting to reabsorb more fluid.

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11
Q

Why are hyaline casts sometimes present within azotemia?

A

A benign finding that suggests minimal flow through the tubules recently.

Does not imply disease.

Formed from Tamm-Horsfall mucoproteins secreted by the tubule.

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12
Q

What are the general S/S associated with prerenal azotemia?

A
  • Uremia (depending on stage)
  • Dehydration/hypovolemia
  • Arrhythmias, cardiomegaly
  • Sepsis
  • Non-specific and diffuse abd pain and ileus
  • Oliguria
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13
Q

What is the general treatment protocol for prerenal azotemia?

A
  • Maintain euvolemia
  • Correct electrolyte abnormalities
  • Avoid nephrotoxic drugs

It is expected that kidney function should be restored if fluid is corrected.

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14
Q

What is the primary underlying etiology of postrenal azotemia and the common complication?

A

Obstruction of renal outflow, resulting in hydronephrosis and damaged renal parenchyma.

Elevation of the intraluminal pressure within the renal pelvis damages the surrounding renal tissue.

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15
Q

What lab findings are typically seen with postrenal obstruction?

A
  • Elevated BUN:Cr > 20:1
  • Urine osmolality: varies, but generally < 400
  • Urine sediment: normal generally.

Urine sediment will depend on what is causing the obstruction, i.e. tumor vs stone.

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16
Q

What generally causes intrinsic kidney injury?

A

Direct damage.

  • Infection
  • Sepsis
  • Nephrotoxins
  • Ischemia

Often will result from prerenal azotemia.

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17
Q

What is the most common type of intrinsic AKI?

A

Acute tubular necrosis.

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18
Q

What are the 3 main underlying etiologies for acute tubular necrosis?

A
  • Ischemia: inadequate GFR and inadequate blood flow => hypoperfusion.
  • Nephrotoxins: exogenous more common.
  • Sepsis: hypoperfusion and direct injury.
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19
Q

What are the most common exogenous nephrotoxins (ABX/Antivirals) that result in acute tubular necrosis?

A
  • Aminoglycosides: occurs even in therapeutic levels. Streptomycin is the least toxic.
  • Amphotericin B: after 2-3g
  • Others: Vanco, sulfa, cephalo, tetra, acyclovir, foscarvir

Trough levels are best for measuring possible nephrotoxicity of aminoglycosides.

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20
Q

What exogenous nephrotoxins can result in acute tubular necrosis? (Excluding ABX and antivirals)

A
  • Radiographic contrast media
  • Chemo/immunosuppresants
  • Heavy metals
  • Ethylene glycol (antifreeze)
  • Insecticides/Herbicides
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21
Q

What is the primary endogenous nephrotoxin that results in acute tubular necrosis?

A

Myoglobinuria, most often from crush injuries or muscle necrosis.

CK generally reads > 20,000.
A result of rhabdo.

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22
Q

How can myoglobinuria be differentiated from hemoglobinuria on UA?

A

Both show Hgb on UA, but myoglobinuria will show NO RBCs.

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23
Q

What is the mainstay treatment for myoglobinuria?

A

Rehydration

Need to monitor electrolyte abnormalities.
Expected that hyperkalemia, hyperuricemia, or hyperphosphatemia may occur.

24
Q

When does hemoglobinuria typically occur in regards to acute tubular necrosis? Tx?

A

Transfusion reactions and hemolytic anemias.

Can be corrected via hydration and treating underlying anemia.

25
Q

When does hyperuricemia typically occur in regards to acute tubular necrosis? Tx?

A

Rapid cell turnover/lysis due to chemo.

Tx: antigout meds.

Intratubular deposition of crystals.

Elevated serum uric acid > 15mg

26
Q

In what condition are bence jones proteins seen in?

A

Multiple myeloma.

Can result in acute tubular necrosis.

27
Q

What lab findings are typical of acute tubular necrosis?

A
  • Hyperkalemia and/or hyperphosphatemia
  • BUN:Cr < 20:1
  • Urine sodium: elevated
  • Urinary sediment: pigmented granular casts or muddy brown.
28
Q

How is acute tubular necrosis treated?

A
  • Removing the underlying cause
  • Avoid volume overload and hyperkalemia.
  • Dietary changes (reduce protein to reduce acidosis)
29
Q

What is the expected prognosis of oliguric vs nonoliguric acute tubular necrosis?

A
  • Oliguric: poorer prognosis, may have permanent reduced kidney function.
  • Nonoliguric: better prognosis but still may never fully recover baseline.

Overall, mortality is 20-50% IP, < 70% in ICU

30
Q

What is the rarest kind of intrinsic AKI and the underlying etiology?

A

Acute glomerulonephritis, due to nephritis.

31
Q

What is the hallmark finding associated with acute glomerulonephritis?

A

Development of inflammatory glomerular lesions in the walls.

Severe is a crescent lesion.

32
Q

What is the classic presentation of acute glomerulonephritis?

A
  • HTN
  • Edema
  • Urine containing proteins, RBCs, WBCs, and RBC casts.
33
Q

What is the underlying etiology of immune mediated acute glomerulonephritis?

A

Development of antigen-antibody complexes in the basement membrane, which are then destroyed by complement.

Destroys basement membrane as well.

Often associated with a recent STREP infection, SLE, or endocarditis.

34
Q

What is the underlying etiology of anti-GBM-associated acute glomerulonephritis?

A

Autoantibodies against the glomerular basement membrane (GBM).

Extension of this to the pulmonary system makes this Goodpasture’s Syndrome.

35
Q

What is the underlying etiology of C3 glomerulopathy?

A
  • C3 deposition in the glomerulus
  • Low serum C3 may imply abnormality in the alternative complement pathway.
36
Q

What is the underlying etiology of monoclonal Ig-mediated glomerulonephritis?

A

Monoclonal Ig deposition in GBM or tubular membrane.
Usually diagnosed with serum protein electrophoresis. (SPEP)

Associated with monoclonal gammopathies.

37
Q

What is the underlying etiology of Pauci-Immune glomerulonephritis?

A

Small vessel vasculitis associated with ANCAs.

Cell-mediated resulting in tissue injury.
No immune complex or Ig or complement formation.
ANCA = antineutrophil cytoplasmic antibody, which are typically screened in vasculitis diseases

38
Q

What are the common etiologies of Pauci-Immune Glomerulonephritis?

A
  • HTN crisis
  • Thrombotic microangiopathies (HUS/TTP)
39
Q

What is the most common finding associated with acute glomerulonephritis? Why?

A

HTN and edema in body parts with low tissue tension. (Scrotal and periorbital)

Peeing out protein = inability to retain fluid within the blood.

40
Q

What lab findings are typically associated with acute glomerulonephritis?

A
  • Elevation of Cr gradually.
  • UA with hematuria and proteinuria
  • Urine sediment: RBCs, WBCs, RBC casts
41
Q

What labs are generally ordered for acute glomerulonephritis to determine the specific etiology?

A
  • Complement levels (C3)
  • ASO titers (recent strep)
  • Anti-GBM antibodies (anti-GBM/goodpasture’s)
  • SPEP (monoclonal)
  • P-ANCA and C-ANCA (Pauci immune)
  • CRP/ESR/ANA
42
Q

What does low C3 & C4 level suggest? C3 alone?

A

C3 & C4: Immune-complex GN

C3: C3 glomerulonephropathy

43
Q

What type of GN is SPEP used to diagnose?

A

Monoclonal Ig-mediated GN

Mainly to check for M-proteins

44
Q

What type of GN are ANCA tests used to diagnose?

A

Pauci-Immune GN

45
Q

What is the general treatment for GN? Specific?

A

General: High-dose corticosteroids

Specific: plasma exchange for goodpasture’s or pauci-immune GN.

46
Q

What is the primary underlying mechanism of acute interstitial nephritis? (AIN)

A

Interstitial inflammatory response, resulting in edema and possible tubular damage.

47
Q

What are the primary causes of AIN?

A
  • Medications (70%), antimicrobials
  • Infections
  • Immunologic (usually will cause GN)
  • Others: allergy, collagen vascular disease

Anything that causes pyelo can cause AIN.

48
Q

What is the classic triad of AIN?

A
  • Fever
  • Rash
  • Arthralgia

All 3 generally present in only 10% of pts.

AIN FAR

49
Q

What lab findings are associated with AIN?

A
  • CBC: eosinophilia
  • Urine sediment: 95% WBCs, minimal proteinuria unless NSAID mediated.
  • Renal Biopsy: inflammatory cells within renal interstitium.

Sediment may also include RBCs, eosinophiluria, and WBC casts.

50
Q

What is the treatment for AIN?

A
  • Removing the underlying cause (usually medication induced)
  • Corticosteroids to reduce inflammation

Generally better recovery and prognosis.

51
Q

What type of AKI is characterized by elevated urine osmolality?

A

Prerenal azotemia

52
Q

What type of AKI typically has elevated fractional excretion of Na?

A

ATN

53
Q

If I find muddy brown casts in my urine sediment, what is the most likely underlying etiology?

A

ATN

54
Q

If I find a few hyaline casts and nothing much in an UA, what type of AKI is most likely?

A

Prerenal azotemia

55
Q

If I see enlarged kidneys on US, what is the most likely AKI?

A

AIN

56
Q

When is a kidney biopsy usually ordered in terms of AKI?

A
  • GN
  • Vasculitis
  • AIN

Usually done once prerenal and postrenal are ruled out, along with ischemic or nephrotoxic AKIs.

GU (14 decks)

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