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Clinical Chemistry (me) > Primary Renal Panel > Flashcards

Primary Renal Panel Flashcards

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1
Q

What makes up the primary renal profile?

A
  1. BUN
  2. Creatinine
  3. Urine SG
  4. Urinalysis
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2
Q

What are the three components of a Urinalysis?

A
  1. Physical Examination
  2. Chemical Examination
  3. Urine Sediment Examination
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3
Q

What makes up the secondary renal profile?

A
  1. Electrolytes
  2. Acid Base
  3. Cholesterol
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4
Q

What are two sources/production of Creatinine?

A
  1. Endogenous production – related to muscle mass

2. Dietary intake (muscle)

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5
Q

How is creatinine excreted from the kidney? From the glomerulus – how is it filtered? Reabsorption?

A

Freely filtered by the glomerulus

No reabsorption by tubules

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6
Q

Is creatinine secreted by the kidney?

A

Generally not but there are a few exceptions
+/- male dogs, humans
++ goats

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7
Q

What is the relationship b/w serum creatinine and GFR?

A

Increase creatinine when decrease GFR

Decrease creatinine when increased GFR

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8
Q

What could explain an increased creatinine?

A

Decrease GFR
Muscle damage
Increase diet intake (minimal)

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9
Q

What could explain a decreased creatinine?

A

Increase GFR

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10
Q

What are the sources for urea? How is it made?

A

Tissue (protein) catabolism
GI (protein) absorption
Protein breakdown –> ammonia –> liver metabolized (urea cycle) –> urea

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11
Q

What could cause tissue (protein) catabolism?

A

Normal turnover
Corticosteroids
Fever

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12
Q

What is more toxic, ammonia or urea?

A

Ammonia&raquo_space; urea

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13
Q

What are some non-renal causes for an increased urea (BUN)?

A 
Enteric hemorrhage (moderate)
High protein diet (minimal)
Terminal starvation -- break down muscle (mild)
\+/- Severe burn -- tissue destruction
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14
Q

What are some non-renal causes for an decreased urea (BUN)?

A

Anorexia/prolonged fasting (mild)
Low protein diets – some prescription Hills (mild)
Decreased liver function (mild to moderate)

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15
Q

What are two routes for BUN excretion?

A

Renal (major)

GI (minor)

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16
Q

How is BUN handled by the kidney? Filtration, reabsorption?

A

All renal handling of BUN –> passive diffusion

Freely filtered by glomerulus
Tubular reabsorption in collecting ducts (40%-60%, depending on flow rate)
Reabsorbed in renal medulla

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17
Q

How does urea play a major role in urine concentration? What determines the efficiency of this process?

A

Urea is reabsorbed by the medulla – aids in water absorption (osmotically)

Slow enough GFR determines how much urea gets reabsorbed – we need enough time for it to diffuse into the interstitium

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18
Q

What clinical sign can influence urea reabsorption?

A

Dehydration
decreased GFR –> increase urea reabsorption –> increase urea in interstitium –> increase water reabsorption due to osmotic pull

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19
Q

How is BUN and GFR related?

A

Increase BUN decrease GFR

Decrease BUN increase GFR

20
Q

When might BUN not be representing GFR?

A

Diet/nutrition low or high in protein

Liver function

21
Q

Azotemia

A

Decrease glomerular filtration

Increased serum nitrogenous wastes (BUN and creatinine)

22
Q

T/F

Azotemia can only happen with renal failure.

A

False
Pre-renal azotemia (dehydration)
Post-renal azotemia (obstruction)

23
Q

What are some clinical signs and lesions that are associate with renal failure and uremia?

A 
Vomiting
Tachypnea (acidosis)
Lethargy (anemia, toxemia)
Anorexia
Diarrhea
Petechiation
Anemia
Mineralization (precipitation of calcium in soft tissue)
24
Q

How is uremia different than azotemia?

A

Uremia – increased nitrogenous wastes in the blood regardless of what the GF is doing.

Azotemia means decreased GF

25
Q

What does it mean when an animal is isosthenuric? How do you decide this? Is it of clinical importance?

A

Urine with solute concentration ~ to plasma
USG = 1.008-1.012
Can occur in healthy animals (w/o renal failure)

26
Q

What is the definition for an adequate USG? What do we consider adequate for USG?
(RED FLAG)

A

The minimum urine specific gravity that is consistently attained in healthy animals when faced with a need for water conservation

Dog: >1.030
Cat: >1.035
Other: >1.025

27
Q

What is a better indicator of GFR, BUN or creatinine? Why?

A

Creatinine because BUN has more extra renal variable to consider.

28
Q

T/F

BUN and creatinine should ALWAYS move together.

A

True

29
Q

Define pre-renal azotemia.

A

Azotemia with adequate urine concentration

30
Q

What are two major mechanisms with initiating factors for pre-renal azotemia?

A
  1. Decreased blood flow to the kidney:
    - Dehydration (vomiting, diarrhea), blood loss
    - Decreased CO, neurogenic shock (vasodilation)
  2. Increased production of nitrogenous wastes
    - High protein diet, GI hemorrhage
    - Increased BUN with normal creatinine
    - SG variable depending on other glomerular filtration influences
31
Q

What are the mechanisms related to causes of pre-renal azotemia?

A

Dehydration, blood loss
– decreased blood volume –> decreased glomerular blood flow

Decreased CO, neurogenic shock
– altered blood flow (with normal or increased total blood volume)

High protein diet, GI hemorrhage

32
Q

Define renal azotemia

A

Azotemia with inadequate urine concentration

33
Q

What is primary renal azotemia?

A

Primary - damage to kidney parenchyma.
“Renal failure” and “Renal insufficiency”
Decreased functional renal mass

34
Q

How much glomeruli and tubule damage is associated with primary renal azotemia?

A

75% glomeruli and 66% tubules in both kidneys

35
Q

What is secondary renal azotemia?

A 
Decreased GFR (pre-renal) with secondary tubular dysfunction (not damage or parenchymal loss!!!)
Loss of functional ability of the tubules
36
Q

What are some mechanisms for cause of secondary renal azotemia?

A
  1. Fluid therapy or diuretics (clinical info should tell you)
  2. ADH deficiency (primary diabetes insipidus) –> no aquaporins –> water loss
  3. Tubules refractory to ADH (secondary diabetes insipidus)
  4. Loss of medullary osmotic gradient (medullary washout)
37
Q

What are cause and mechanism for secondary diabetes insipidus leading to secondary renal azotemia?

A
  1. Hypercalcemia
    Affects ADH release
    Correction may restore renal fxn
  2. Pyometra (toxin)
    interferes with ADH if at level of kidney
  3. Pyelonephritis (toxin)
  4. Hypokalemia (especially cats with CRD)
    Restore potassium – may correct secondary while leaving primary as a remaining issue
  5. Cushing’s disease
    glucocorticoid interferance with ADH receptor
    Kidney can usually overcome this
38
Q

Explain what medullary washout means.

What will we first recognize clinically on the biochem?

A

Loss of medullary osmotic gradient (sodium and urea) in the medullary interstitium.
Commonly seen with PU/PD from increased GFR causing less time for urea and sodium to diffuse into the medulla.
Aquaporins are functioning but we have nothing to pull/reabsorb water

Severe hyponatremia

39
Q

What is the difference in px for primary versus secondary renal azotemia?

A

Primary

  • Guarded
  • Depends on reversibility of insult and compensatory ability of remaining nephrons

Secondary

  • Favorable to Excellent
  • Depends on restoring renal blood flow, recognizing it as secondary RA, and correcting underlying primary process
40
Q

What is the most common causes of hypercalcemia leading to secondary renal azotemia?

A

Humoral hypercalcemia of malignancy (HHM)

  • Anal sac carcinoma
  • Lymphoma
41
Q

Define post renal azotemia

A

Azotemia with variable urine concentration

42
Q

What are causes of post renal azotemia?

A 
Obstruction/breach in post renal urinary tract
- urinary calculi
- ruptured bladder
- torn ureter/urethra
congenital malformations
43
Q

BUN or Creatinine? Why?

Sensitivity for decreased glomerular filtration.

A

Both

Decreased glomerular filtration is azotemia, you only see azotemia with 75% loss of kidney fxn. Both will be high

44
Q

BUN or Creatinine? Why?

Specificity as a measure of GF

A

Creatinine

Less extra renal variables

45
Q

What is increased cholesterol commonly associated with in renal disease/failure?

A

Primarily associated with hypoalbuminemia –> decreased oncotic pressure –> liver produces more lipoproteins (cholesterol) to compensate

46
Q

What are important disease differentials for increase cholesterol?

A 
Renal disease (protein losing nephropathy) -- only associated with RENAL protein loss!
Hepatobiliary disease (cholestasis)
Pancreatitis
Diabetes mellitus
Cushing's disease
Hypothyroidism
47
Q

What are causes for decreased cholesterol?

A

Decreased hepatic production/functional mass

Clinical Chemistry (me) (4 decks)

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