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Clinical Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Renal Function

A
  • Clear metabolic wastes from blood
  • Conserve nutrients
    • glucose
    • protein
  • Maintain water, electrolyte, and acid-base balance
  • Hormone production
    • erythropoietin
    • Vitamin D
    • Renin
  • Hormone degredation/excretion
  • Enzyme degradation / Excretion
    • amylase, lipase
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2
Q

Healthy Glomerulus:

Stays in blood

A

Cells: RBC, WBC, Platelets

Plasma proteins (albumin)

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3
Q

Healthy Glomerulus:

Passes thru barrier

A

water

solutes: electrolytes, glucose, urea, small proteins

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4
Q

Healthy Glomerulus:

What determins what gets through

A

size: >68,000 not filtered

Charge: Basement membrane negatively charged, Negatively charged molecules may be repelled

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5
Q

Physiologic Functions of the Nephron:

Glomerular filtration

A

Passive:

Substances move from plasma to tubules

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6
Q

Physiologic Function of the nephron:

Tubular resorption

A

Passive and Active:

Solutes move from tubules to plasma

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7
Q

Physiologic Functions of Nephron:

Tubular secretion

A

Passive and Active:

Substances move from plasma to tubules

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8
Q

Physiologic function of Nephron:

Water regulation

A

Maintain water balance, May go to or from the plasma

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9
Q

Glomerular Filtration Rate (GFR)

A

Volume of plasma filtered form glomerular capillaries into bowman’s space per unit time

Measured by determining rate of clearance of a substance from plasma

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10
Q

Glomerular Filtration Rate:

Dependent on?

A

Renal blood flow

of functional nephrons

Hydrostatic pressure in Bowman’s capsule

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11
Q

Osmometer

A

Measures osmolality

Freezing point assay, not convenient, but more accurate

Measure depends on the number of particles in a volume of water

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12
Q

Refractometer

A

Measures Urine specific Gravity

Depends ofn particle weight and how each particle bends light

Prone to interference

Differences between how glucose, electrolytes, urea, proteins, lipids, and other substances refract light

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13
Q

Antidiuretic Hormone (ADH)

A

Synonym: Vasopressin

Synthesized in the hypothalamus

Secreted form the posterior pituitary glands

Interacts with receptors ont he cells of hte distal tubules and collecting ducts

Opens water channels via aquaporin proteins

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14
Q

Stimuli for ADH secretion

A

Plasma hyperosmolality

Decreased cardiovascular pressure

increased concentration of angiotensin

Result: Conserve body water to decrease plasma osmolality and increase blood volume

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15
Q

Major events of Nephron Segments:

Proximal Tubule

A

Revomes volume

No change in concentration

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16
Q

Major events of nephron segments

Descending Loop of Henle

A

Removes water

Increases concentration

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17
Q

Major Events of Nephron Segments”

Ascending Loop of Henle

A

removes solutes

Dilutes (decreases concentration)

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18
Q

Major events of Nephron segments

Distal nephron

A

removes water

Increases concentration

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19
Q

To produce conentrated Urine

A

Adequate number of functional nephrons

Adequate production of ADH from pituitary

Distal nephron epithelial cells must be responsive to ADH

Hypertonic interstitium in the renal medulla

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20
Q

Anuria

A

Lack of urine production

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21
Q

dysuria

A

painful or difficult urination

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22
Q

oliguria

A

production of an abnormally small amount of urine

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23
Q

Pollakiuria

A

indicating increased frequency of urination. Doesn’t indicate urine volumes

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24
Q

Polydipsia

A

increased water consumption

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25
Q

Polyuria

A

production of excessive amounts of urine

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26
Q

Azotemia

A

Increased concentration of Urea Nitrogen and/or creatinine

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27
Q

Urea Nitrogen

A

Urea diffuses readily across most cell membranes along a concentration gradient

Rapid equilibrium amont intercellular and extracellular fluid compartemnts (~90)

Whole blood urea nitrogen = serum urea nitrogen

Urea contributes to the renal medullary concentration gradient

This drives recovery of water / cocnentration of urine in the collecting ducts

28
Q

Creatinine Metabolism

A

Creatinine is a wast product from the normal breakdown of musscle tissue

Freely filtered thru glomerular barrier into ultrafiltrate

NOT RESORBED BY TUBULES
excreted in urine

29
Q

Urea Nitrogen Assay

A

Serum or plasma

Stable for 1 day at room temp

203 months if frozen

30
Q

Creatinine Assay

A

Serum or plasma (NO whole blood)

31
Q

Increased Creatinine (Ct)

A

Decreased GFR

32
Q

Decreased Creatinine

A

May not be clinically significant

Consider:

Decreased muscle mass

Hypoproteinemia

33
Q

Pre-Renal Azotemia

A

UN and creatinine are increased

Urine is concentrated

34
Q

Pre-renal Azotemia:

Possible Causes:

A
  • Decreased Renal Blood Flow = decreased GFR
    • Dehydration
    • hypovolemia / fluid maldistribution
    • Severly decreased cardiac output
  • Increased production of urea / creatinine
    • Urea:
      • high protein diet
      • GI hemorrhage
    • Cretinine:
      • heavily muscled animals
35
Q

Renal Azotemia

A

Primary causes is within the nephron

UN and creatinine are increased

Urine is NOT concentrated in the face of dehydration

decreased concentrating ability

Isothenuric urine (1.007-1.013) indicates an inability to concentrate and dilute

36
Q

Post-renal Azotemia

A

Primary problem is after the nephron

Problem that interferes with excretion

UN and creatinine are increased

37
Q

Uremia

A

Cliical Syndrome associated with renal failure

Azotemia plus severe physical consequences fo renal failure

  • Polyuria / polydipsia
  • Vomiting / diarrhea
  • Ammonia odor of breath
  • GI ulcers
  • Nonregenerative anemia
  • Weight loss
  • Convulsions
  • Coma
38
Q

Abnormal Laboratory Results in Azotemic Animals:

Sodium and chloride

A

increased with prerenal azotemia

Low or WRI with renal failure due to decreased resorption

39
Q

Abnormal Laboratory Results in Azotemic Animals:

Potassium

A

Usually high in oliguric and anuric renal failure

Low in cats and cows with polyuric renal failure

40
Q

Abnormal Laboratory Results in Azotemic Animals:

Phosphate

A

Excretion is decreased when GFR is decreased for any reason (Prerenal, renal, postrenal)

Usually high in animals with moderates to marked azotemia

41
Q

Abnormal Laboratory Results in Azotemic Animals:

Magnesium

A

Increased with decreased GFR

42
Q

Abnormal Laboratory Results in Azotemic Animals:

Calcium:

Dogs, cats, cows

A

Usually WRI or slightly decreased with renal failure

Hypercalcemia in dogs and cats with azotemia is more likely to be the cuase for renal disease then the result of renal disease

43
Q

Abnormal Laboratory Results in Azotemic Animals:

Calcium:

Horses

A

Rely on renal excretion of calcium

Calcium is high in most horses with renal failure due to decreased excretion and a species difference in calcium metabolism

44
Q

Abnormal Laboratory Results in Azotemic Animals:

Hematocrit

A

WRI or high in pre-renal azotemia and ARF

Non-regenerative anemia in CRF

45
Q

Abnormal Laboratory Results in Azotemic Animals:

Total Protein, Albumin

A

WRI or high in pre-renal azotemia +/- ARF

Within reference interval or low in CRF

46
Q

Abnormal Laboratory Results in Azotemic Animals:

Acid/base abnormalities

A

Yes!

47
Q

Mechanisms of Polyuria

A
  1. Lack of ADH production
    1. central diabetes insipidus
    2. Phychogenic polydipsia
  2. Distal tubule/Collecting Duct cells cannot respond ot ADH
    1. nephrogenic biabetes insipidus
  3. Must be a conentration gradient between tubular fluid and interstitium
    1. solute diuresis
    2. Reduced medullary intersitium osmolality
48
Q

Major initial/primary pathogenic mechanisms for Polyuria Chart

A
49
Q

Decreased Renal Reserve

A

GFR is about 50% of normal capacity

Clinically healthy: NOT azotemic or polyuric – susceptible to insult

50
Q

Chronic Renal Insufficiency

A

25-50% function

Azotemic, Anemia, Decreased concentrating ability, Polyuria

51
Q

Chronic Renal Failure

A

<20-25% function

Azotemic, anemia, decreased concentrating ability,

Electrolyte imbalance, clinical signs fo uremia

52
Q

End-Stage Renal disease:

A

<5% function

Terminal uremia signs and oliguria or anuria

53
Q

Causes of Polyuria in Chronic Renal Disease?

A

Loos of functional nephrons

  • More solute presented to remaining functional nephrons
    • Increased load through nephrons
    • Solute diuresis
  • Medullary hypertonicity is not maintained
    • medullary tissue damage or abnormal blood flow
    • Decreased sodium, chloride and urea reabsorption
  • Damaged cells less responsive to ADH
54
Q

Acute Renal Failure

A

Reversible or Irreversible

Abrupt insult or disease

Marked decrease in GFR → Azotemia → Uremia

Degree of azotemia does NOT differentiate chronic vs. acute

Toxins, ischemia, infection

Vascular supply, glomerular, tubular, interstitial disease

55
Q

Mechanisms of Proteinuria:

Hemorrhagic or inflammatory

A

This is the most common mechanism for addition of protein to urine

Hemorrhage anywhere in the urinary tract

Inflammation causing exudation of plasma proteins intohte urinary tract

Magnitide of Proteinuria varies but it DOES NOT lead to hypoalbuminemia

56
Q

Mechanisms of Proteinuria:

Funcitonal

A

Transient mild increase in urine protein content

Exercise, fever, seizures, stress

Mechanism unclear

57
Q

Mechanism of Proteinuria

Overload

A

Increased plasma concentration of small protiens that pass through glomerular filtration barrier and exceed capacity for tubular resorption

Hemoglobin, myoglobin, immunoglobin light chains,

Overload proteinuria DOES NOT lead ot hypoproteinemia

58
Q

Mechanisms of Proteinuria:

Tubular

A

Proximal tubular injury causing failure to reabsorb small proteins

Usually associated with Acute renal tubule damage

Tubular damage = exposure to neprothoxins

DOES NOT result in hypoproteinemia

59
Q

Mechanisms of Proteinuria:

Glomerular

A
  • Damage/disruption of the glomerular filtration barrier
    • immune complex deposition
    • Amyloid deposition
    • Inflammatory cells contribute - release cytokines and other mediators that can damage the glomerulus
  • Increased permeability to large and or negatively charged proteins
    • albumin first, globulins later with progressiive damage
    • Glomerular damage often leads to sleective hypoproteinemia
  • Progressive glomerular disease
    • can lead to tubular damage and tubular proteinuria, loss of nephrons → azotemia, renal failure
60
Q

Severe Glomerular Disease

A

The entire nephron may become nonfuncitonal

Severe, persistent proteinuria can lead to the nephrotic syndrome

Proteinuria

hypoproteinemia

Hypercholesterolemia

Ascited or edema

61
Q

Urine Protein:

Urine Creatinine Ratio:

UPC < 0.2

A

Healthy dogs and cats

62
Q

Urine Protein:

Urine Creatinine Ratio:

UPC 0.1-0.4, 0.1-0.5

A

Is borderline - not conclusive evidence of proteinuric renal disease

63
Q

Urine Protein:

Urine Creatinine Ratio:

0.4-3, 0.5-3

A

Proteinuria is present

in this range proteinuria could result form glomerular or tubular damage

64
Q

Urine Protein:

Urine Creatinine Ratio:

UPC >3

A

Indicative of glomerular disease

Tubular disease may also be present, but it is not the whole story

65
Q

Urine Protein:

Urine Creatinine Ratio:

UPC ~15

A

Most indicative of amyloidosis

Clinical Pathology (20 decks)

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