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UA Spring > Renal disease pt 2 > Flashcards

Renal disease pt 2 Flashcards

(56 cards)

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1
Q

How does the liver compensate for loss of albumin? Caveat?

A

Make lipoproteins/lipids to restore oncotic pressure, but lipids are small and can end up in urine

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2
Q

Nephrotic syndrome UA findings

A
  • Massive proteinuria > 3.5 g/dL
  • Low levels of serum albumin
  • High levels of serum lipids
  • Pronounced edema
  • RBC
  • Fat droplets
  • RTE
  • Epithelial casts
  • Fatty casts
  • Waxy casts
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3
Q

Why is there edema in nephrotic syndrome?

A
  • Loss of albumin reduces oncotic pressure such that water leaves capillaries to the tissues
  • Tissues are hypertonic to blood, so water leaves to tissues
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4
Q

Minimal Change Disease aka

A

Liver nephrosis

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5
Q

What happens in minimal change disease?

A

Little cellular change, thus allowing some proteins to pass through glomerulus

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6
Q

Minimal change disease typically found in

A

Children

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7
Q

Minimal change disease clinical findings

A
  • Edema
  • Fat droplets
  • Marked proteinuria
  • Transient hematuria
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8
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

Affects only certain glomeruli, others can stay normal

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9
Q

FSGS features what kind of deposits?

A

Immune deposits of IgM and C3 (complement)

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10
Q

FSGS UA findings

A
  • Elevated protein
  • RBC
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11
Q

Alport Syndrome

A
  • Inherited disorder affecting glomerular basement membrane (GBM)
  • GBM thin, no antibody effect
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12
Q

Alport syndrome symptoms

A
  • Same as nephrotic syndrome
  • Massive proteinuria > 3.5 g/dL
  • Low levels of serum albumin
  • High levels of serum lipids
  • Pronounced edema
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13
Q

Most common cause of end-stage renal disease

A

Diabetic Nephropathy

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14
Q

How does damage occur in diabetic nephropathy?

A
  1. Glomerular membrane thickening
  2. Mesangial cell proliferation
  3. Increased deposition of cellular material
  4. Vascular sclerosis
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15
Q

Diabetic nephropathy features what kind of deposits and where?

A

Glycosylated proteins deposit in capillary tufts

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16
Q

List tubular disorders

A
  • Fanconi Syndrome
  • Nephrogenic diabetes insipidus
  • Renal glycosuria
  • Acute tubular necrosis
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17
Q

Acute tubular necrosis features

A

RTE cell damage

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18
Q

Causes of acute tubular necrosis

A
  • Ischemia (reduced blood flow/lack of oxygen) due to surgery, trauma, or shock
  • Toxic substances (aminoglycosides, anti-fungals, radiographic dye, anti-freeze, heavy metals, Hgb, Mgb
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19
Q

Acute tubular necrosis UA findings

A
  • Hallmark: RTE cells and RTE casts
  • Mild proteinuria
  • Wide variety of casts (granular, waxy, broad)
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20
Q

Fanconi’s syndrome

A

Failure of tubular reabsorption in PCT, which means there’s disrupted transport, cellular energy, and membrane permeability

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21
Q

Substances affected in Fanconi’s syndrome

A
  • Glucose
  • Amino acids
  • Phosphorus
  • Sodium
  • Potassium
  • Bicarb
  • Water
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22
Q

List an inherited cause of Fanconi’s syndrome

A

Wilson’s disease

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23
Q

List an acquired cause of Fanconi’s syndrome

Study These Flashcards
A

Multiple Myeloma

24
Q

List an exogenous cause of Fanconi’s syndrome

25
Nephrogenic Diabetes Insipidus
Inability of tubules to respond to ADH
26
Nephrogenic Diabetes Insipidus UA findings
- Low specific gravity - Frequent urination
27
Renal glycosuria
- Inherited disorder where glucose receptor on PCT cell won't work or not enough expressed - Only glucose reabsorption affected
28
Serum and urine glucose levels in renal glycosuria
- Serum glucose = normal - Urine glucose = increased
29
Most common renal disease
UTI (upper or lower)
30
Interstitial disease affects
The interstitium and tubules
31
Most common interstitial disorder
Cystitis (bladder infection)
32
Cystitis UA findings
- Numerous WBC - Numerous bacteria - Mild proteinuria - RBC (not from glomerulus)
33
Pyelonephritis
**Upper** UTI
34
Acute pyelonephritis result of
Bacteria ascending upwards from lower UTI due to renal calculi, pregnancy, or reflux of urine
35
Acute pyelonephritis symptoms
- Urination frequency - Burning - Lower back pain - Correlation btwn acute pyelonephritis and bacteremia
36
Acute pyelonephritis UA findings
- Numerous WBC - Numerous bacteria - Proteinuria - **WBC casts** (tubule infection)
37
How to distinguish between upper and lower UTI?
Upper UTI = casts present (WBC) because only nephron makes casts and bladder (lower UTI) can't
38
More serious form of pyelonephritis
Chronic
39
Chronic pyelonephritis often diagnosed in
Children (poorly formed kidneys)
40
Chronic pyelonephritis congenital urinary structural defect effects
- Bladder reflux to ureters or renal pelvis - Cannot empty collecting ducts
41
What can lead to chronic renal failure?
Permanent tubular damage
42
UA findings in chronic pyelonephritis
- Numerous WBC - Bacteria - **WBC casts** - Granular casts - Waxy casts - Broad casts
43
Acute interstitial nephritis
- Inflammation of renal interstitium or tubules - Associated with allergic reaction to meds (penicillin class, sulfonamides, cephalosporin, NSAIDs)
44
Acute interstitial nephritis UA findings
- **No bacteria** - **Eosinophils** (do Hansel stain) - RBC - Proteinuria - Numerous WBC - WBC casts
45
Final progression to end-stage renal failure looks like:
- Marked GFR reduction (<25ml/min) - Steady increase serum BUN/creatinine - Electrolyte imbalance - Lack of renal concentrating ability - Positive urine protein/glucose - Increase granular, waxy, and broad casts
46
Acute vs chronic renal failure
Acute renal failure shows **sudden** loss of renal function and is frequently **reversible**
47
Pre-renal causes of renal failure
Sudden reduction in blood flow
48
Renal causes of renal failure
Acute glomerular or tubular disease
49
Post-renal causes of renal failure
Renal calculi or tumor obstructions
50
Acute renal failure general rule of thumb UA findings
- RTE cells + casts = acute tubular necrosis - WBC casts = interstitial infection of inflammation - Abnormal cells = malignancy
51
Renal lithiasis
- Kidney stones that form in the kidney, ureters, and bladder - Calculi vary in size
52
Conditions favoring kidney stone formation
- pH - Chem concentration - Urinary stasis - Presence of certain crystals
53
75% of kidney stones consist of
Calcium oxalate or phosphates
54
Other kidney stones may consist of
Mag-ammonium phosphate, uric acid, cystine
55
Patient management of kidney stones
- Maintaining urine pH to prevent crystallization - Hydration - Dietary restrictions
56
Renal lithiasis UA findings
Microscopic RBC due to irritation of the tissue by kidney stone (aka calculus)

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