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CDM exam 2 > Renal Material > Flashcards

Renal Material Flashcards

(50 cards)

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1
Q

Things to look for to determine Prerenal

A 
20:1 BUN/Scr ratio
increase of BUN rapidly
no evidence of cell death
no RBC
no WBC
Urine Na < 20mEq/L
FeNA % <1 (conserving)
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2
Q

Things to look for to determine Intrarenal

A 
16:1 BUN/Scr ratio
Scr doubles, BUN increases (not as rapidly as prerenal)
muddy brown casts 
RBC, WBC
Urine Na >40 mEq/L
FeNA% >2 (wasting)
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3
Q

Things to look for to determine Postrenal

A 
16:1 ratio BUN/Scr
cellular debris
RBC -variable
WBC -1+
>40 mEq/L
FeNA% >2 (wasting) 
blockage/ obstruction
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4
Q

Prerenal AKI also known as

A

Prerenal Azotemia

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5
Q

Prerenal involves changes in

A

Volume and tone

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6
Q

Prerenal occurs in

A

afferent and efferent arterioles (Glomerulus)

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7
Q

Risk factors for prerenal

A 
Age
Diuretic use 
Poor oral intake 
GI fluid loss
CHF
Renal Artery Stenosis
ACEi/ARBs
NSAIDs
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8
Q

Prerenal Treatment

A

Fluid replacement with NaCl

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9
Q

Intrinsic kidney injury also known as

A

Intrarenal AKI

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10
Q

What is intrinsic kidney injury

A

structural damage to glomerulus, tubules or interstitium which often occur due to prolonged prerenal causes

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11
Q

Intrinsic kidney injury leads to

A

renal cell necrosis by mechanisms of ischemia, infection or immune response that result in inflammation

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12
Q

3 types of intrinsic kidney injury

A

Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN)
Glomerulonephritis

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13
Q

Diagnosing with ATN

A

muddy brown casts
epithelial cells
no crystals
mild proteinuria (

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14
Q

Diagnosing with AIN

A

WBC casts, eosinophilic casts
WBCs 2-4+, eosinophils
No crystals
mild proteinuria (

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15
Q

Diagnosing with Glomerulonephritis

A 
RBC casts 
RBCs
Crystals may be present
moderate-large proteinuria (.5-3g/day or >3g/day)
slower development over 7-10 days
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16
Q

Drug induced postrenal AKI

A

Common drug causes include acyclovir, indinavir, sulfadiazine, chemotherapy causing high cell turnover (e.g., uric acid nephropathy)

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17
Q

kidney calculi (kidney stones)

A

Nephrolithiasis: the process of forming kidney stones
May or may not lead to postrenal obstruction
Who develops?
Family history of calcium oxalate stones or urate stones
Diabetes, gout, obesity
Leads to flank pain and hematuria; may lead to renal obstruction
Prevention is key through hydration and dietary modifications (low oxalate and low urate containing foods)

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18
Q

AKI clues:

Tenting of skin

A

prerenal

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19
Q

AKI clues:

Dark urine

A

prerenal

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20
Q

AKI clues:

Fever/high WBC

A

AIN or Glomerulonephritis

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21
Q

AKI clues:

Fever/Rash

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A

AIN or Glomerulonephritis

22
Q

AKI clues:

Blood in urine

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A

Glomerulonephritis or postrenal obstruction (kidney stones)

23
Q

Kidney regulatory function

Study These Flashcards
A

Control composition and volume of blood volume

Maintain stable concentrations of cations such as sodium (Na), potassium (K), and calcium (Ca)

Maintain acid-base balance

24
Q

Kidney Excretory function

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A

Produce urine

Remove metabolic waste (e.g., urea and other waste products)

25
Kidney Hormone function
Produce renin for BP control Produce erythropoietin which stimulates marrow production of red blood cells Activate 25(OH)-D (inactive vitamin D)  1,25(OH)2D (active vitamin D)
26
Kidney Metabolic function
Gluconeogenesis Metabolize drugs and endogenous substances (e.g., insulin)
27
Normal kidney sodium reabsoprtion
Normal kidney = 99% of sodium is reabsorbed with a net loss of 1% or less into urine
28
Afferent Arteriole
Looking at volume and tone
29
Efferent Arteriole
looking at tone
30
What is AKI?
200% increase of the serum creatinine over 24 hours Acute ↑ in creatinine with or without↓ in urine output over a short period of time
31
Nonoliguria
urine output > 500 mL in 24-hours (per day)
32
oliguria
Urine output 100-500 mL in 24-hours (per day)
33
Anuria
urine output < 100 mL in 24-hours (per day)
34
Non-modifiable risk factors for AKI
``` Chronic kidney disease Diabetes Older age Chronic liver disease (e.g., cirrhosis) Congestive heart failure (CHF) Renal artery stenosis Peripheral vascular disease ```
35
Modifiable risk factors for AKI
``` Volume depletion (e.g., poor oral intake/dehydration, diarrhea, vomiting) Hypertension/Hypotension Hypoalbuminemia Sepsis/shock Nephrotoxic medications Major surgery/anesthesia ```
36
Drugs associated with prerenal AKI
``` ACEi/ARBs * NASAIDs * Cyclosporine Tacrolimus SGLT-2 inhibitors ```
37
impaired regulation with NSAIDs in prerenal
NSAIDs inhibit prostaglandins --> constriction of afferent arteriole -> reduced flow and pressure --> decreased perfusion pressure and filtration
38
impaired regulation with ACEi/ARBs
ACEi/ARBs block angiotensin 2 --> dilation of efferent arterioles --> reduction in back pressure --> decrease perfusion pressure and filtration
39
Drugs associated with ATN
Radiocontrast media | Aminoglycosides (AG)
40
Contrast induced nephropathy (CIN)
↑ in SCr by ≥0.5 mg/dL or 25% from baseline Usually begins 24-48 hrs post-procedure; Peaks in 3-5 days and begins downtrending; Returns to baseline in 7-10 days
41
CIN risk factors
``` Age anemia HF hypotension volume depletion ```
42
drug induced ATN
Major cause of drug-induced ATN Variable incidence of nephrotoxicity, 1.7-58% Onset: 5-10 days after initiation of therapy; serious; largely preventable Proposed pathogenic mechanism Cationic charge (heavily filtered into tubule)  binding and uptake by PCT cells  disrupt normal cell function  tubular cell death Stimulate Ca sensing receptor in the apical membrane  induction of cellular signaling and cell death Presentation: ATN (oliguric or non-oliguric), magnesium wasting, FeNa >2%, presence of muddy brown casts
43
ATN MOA
rupture proximal tubular epithelial cell
44
ATN patient related risk factors
``` CKD Advanced age Liver disease Dehydration Hypotension Magnesium or potassium deficiencies ```
45
ATN drug related risk factors
``` Prolonged course Cumulative dose Trough concentration >2 mcg/mL Repeated courses (14-day wash out) Concomitant nephrotoxic agents ```
46
Drugs associated with AIN
Allergenic medication | penicillins, cephalosporins, fluoroquinolones, sulfamides, NSAIDs, PPIs
47
Drug induced AIN onset
7-20 days due to sensitizing
48
drug induced AIN treatment
Stop drug and start prednisone 1 mg/kg/day
49
Drugs associated with Postrenal
Acyclovir Sulfonamides Indinavir
50
Management of DIKD
stop offending agent avoid nephrotoxins maintain hydration

CDM exam 2 (12 decks)

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