• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/26

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

26 Cards in this Set

  • Front
  • Back
Which of the following is false about the RIFLE definition of AKI?
a) serum creatinine, GFR, and urine output are used to grade severity
b) End stage kidney disease is greater than 3 months loss of renal function
c) Loss and ESKD are used to grade severity
d) RIFL are on a bi-directional continuum and stage can change any day
c) Loss and ESKD are used to grade severity

Loss and ESKD are used to grade outcome
Risk, injury and failure are used to grade severity
What are the urine volume/day for oliguria and anuria? What is the significance of non-oliguiric AKI?
Oliguiria: <400 ml/day
Anuria: <100 ml/day

Non-oliguric AKI has better outcomes than AKI with oliguria or anuria.
What is the standard approach to AKI? Approx. how prevalent are each of these causes of AKI?
"Pre-renal (decreased perfusion, normal nephron structure and function) - 20-30%

Renal (abnormal structure and function of nephrons) - 50-60%

Post-renal/obstructive (urine outflow passages are blocked and secondarily abnormal function of the...
Pre-renal (decreased perfusion, normal nephron structure and function) - 20-30%

Renal (abnormal structure and function of nephrons) - 50-60%

Post-renal/obstructive (urine outflow passages are blocked and secondarily abnormal function of the nephrons) - 10%
What does a low fractional excretion of sodium [FeNa] (<1%) indicate? High (>2%)?
Low FeNa means normal tubular reabsorption [type of AKI: pre-renal or early post-renal]

High FeNa means sodium wasting from intrarenal damage. [type of AKI: ATN, late post-renal]
What are some causes of pre-renal AKI?
-Decreased intravascular volume -extracellular volume depletion [diarrhea, vomit, diueretics, bleed] or decreased effective circulating volume [CHF cirrhosis, nephrosis, peritonitis, sepsis]
Hypotension
-decreased CO [tamponade, sepsis]
-Impaired renal vasculature - renal artery embolus or occlusion; Increased resistance in afferent-efferent arterioles: (NSAIDs, anesthesia.)
-Decreased intraglomerular pressure - ACEi, ARBs
vasoconstricting drugs - cyclosporin
What is the prognosis of pre-renal AKI?
Usually reversible if renal blood flow restored and volume status is corrected quickly.

However, if prolonged, can progress to intrarenal kidney damage.
If a person's had a normal sodium reabsorption [FeNa], normal urine concentrating ability and a normal urine pH, what type of AKI might they have?
Pre-renal
Also, negative urinalysis for RBC, WBC, proteinuria
What are post-renal causes of AKI?
Bilateral ureteric obstruction
- intraureteral - stones, clots
- extraureteral - bladder/prostate/cervical ca
Bladder neck obstruction
- prostate bladder ca
- autonomic nueropathy
What are some ways to manage pre-renal AKI?
Maintain normal BP, CO
Maintain euvolemia/IV fluids
Avoid nephrotoxins
Hold ACEi, ARB, NSAIDs
Tx sepsis
What is involved in the management of post-renal AKI?
Insert urinary Foley catheter
Urology and radiology for UT obstruction (lithotripsy, trans-pubic catheter)
Monitor volume status
What is a 3 category approach to intra-renal AKI?
Glomerular
TubularoInterstital
Vascular
What is a diagnostic urinalysis for RPGN?
1. RBC casts
2. dysmorphic RBC
3. protein
What are causes of rapidly progressing glomerular nephritis?

and what are they categorized by?
1. Pauci-immune (aka vasculitis) (90%)
2. Anti-GBM (8%)
3. Immune complex mediated (2%)

immunofluorescence
What are 3 types of vasculitis that cause inflammation of the blood vessels?
i) granulomatosis with polyangitis (GPA)
ii) microscopic polyangitis/arteritis (MPA)
iii) Churg-Straus
Match the lab test to the RPGN disease.
GPA, Microscopic polyangitis, Churg-Straus, Anti-GBM disease

LAB TESTS:
+anti GBM antibodies
+ve anti-MPO
+ve antiproteinase (c-ANCA)"
GPA -anti-proteinase (c-ANCA)
Microscopic polyangitis - +ve anti-MPO
Churg-Straus (none specified)
Anti-GBM disease anti- GBM & sometimes +ve cANCA
What are symptoms of Churg-Straus?
Multi-organ system involvement
Predominant worsening of asthma
(rare)
Which disease affects middle age men & women and presents with up. reps tract (nose/sinus, throat), lungs & kidney symptoms?
Granulomatosis with polyangitis (GPA)
What are some common conditions associtated with immune complex mediated disease causing RPGN?
Lupus
IgA disease
Membranoproliferative disease (hep b/c)
Post infectious glomerulonephritis
If a patient had non-specific symptoms (i.e. fever, weight loss, myalgias), but also had sudden renal failure or pulmonary hemorrhage, and/or skin, CNS and GI tract symptoms, which vasculitis would most likely be present?
Microscopic polyangitis
What's the most predominant symptom of Churg-Strauss?
worsening of asthmatic symptoms
What is the name of the syndrome where antibodies attack capillaries in aveolar walls?
Good pasture's syndrome
What are some symptoms in anti-GBM?

what's the pathophys?
hemoptysis, fever, wt loss, n/v, renal failure

lab: +ve ANCA in some and anti-GBM antibodies usually present

antibodies against the the GBM, in the lungs the antibodies attack the alveolar walls
Why is a renal biopsy needed for RPGN and in the biopsy, what may indicate severe glomerular injury?
"Used for definitive diagnosis

Crescents=sign of severe glomerular injury. They are an accumulation of epithelial cells and circulatory monocytes/macrophages in Bowman's space."
Used for definitive diagnosis

Crescents=sign of severe glomerular injury. They are an accumulation of epithelial cells and circulatory monocytes/macrophages in Bowman's space."
What are the absolute indications for dialysis?
Acidosis
Electrolytes: hyperkalemia, hypercalcemia
Intoxication (ASA, toxic EtOH, Li)
Overload (volume)
Uremic encephalopathy, pericarditis, pleuritis

AEO - when refractory to medical treatment
What is the specific management for ANCA+ anti-GBM?
Immunosuppressive therapy +/- plasmaphoresis
What are some of the toxicities/side effects to be aware of in the treatment of RPGN?
Cyclophosphamide: amenorrhea, cystitis, bladder cancer

Prednisone: fractures, diabetes, cataracts

Opportunistic infections: 6% pneumocystis carinii pneumonia. Use prophylactic trimethoprim-sulfamethothoxazole 3X/week