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crf Flashcards

1
Q

between cats and dogs,in which is renal dz common

A

cats

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2
Q

causes of srf in dogs

A
  • Chronic tubulointerstitialnephritis of unknown cause
  • Chronic pyelonephritis
  • Chronic glomerulonephritis
  • Amyloidosis
  • Familial renal diseases
  • Hypercalcemicnephropathy
  • Chronic obstruction (hydronephrosis)
  • Sequel to acute renal disease (e.g., leptospirosis)
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3
Q

% of geriatric dogs affected by crf

A

CRF may affect 0.5 to 1.0% of the geriatric canine population

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4
Q

causes of crf in cats

A
  • Chronic tubulointerstitialnephritis of unknown cause
  • Chronic pyelonephritis
  • Chronic glomerulonephritis
  • Amyloidosis
  • Familial renal diseases
  • Hypercalcemicnephropathy
  • Chronic obstruction (hydronephrosis)
  • Sequel to acute renal disease (e.g., leptospirosis)
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5
Q

% of geriatric cats affected by crf

A

CRF may affect 1.0 to 3.0% of the geriatric feline population

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6
Q

Clinical History in CRFF

A
  • they are non specific

Polyuria/ polydipsia(common)

  • Vomiting (dogs)
  • Inappetance/ Anorexia
  • Weight loss
  • Lethargy
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7
Q

physical findings in crf

A
  • Weight loss / low BCS
  • Poor haircoat
  • Oral lesions (dogs > cats)
  • Pale MM
  • Dehydration
  • Osteodystrophy(young growing dogs with familial renal disease)
  • Small / irregular kidneys (may be normal)
  • Ascites/ edema (consider glomerulardisease)
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8
Q

Laboratory Findings in CRF

A
  • Nonregenerativeanemia / lymphopenia
  • Isosthenuria(67% loss of nephrons)
  • Azotemia(75% loss of nephrons)

Hyperphosphatemia(85% loss of nephrons)

  • Decreased serum HCO3-
  • Variable serum Ca+2
  • Mild hyperglycemia
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9
Q

Anemia of CRF

A
  • Nonregenerative(normochromic, normocytic)
  • Variable in magnitude and correlated with severity of CRF (creatinine)
  • Serum EPO concentrations are low to normal (inappropriate for PCV)
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10
Q

Pathophysiologyof CKD / CRF:Trigger-Point Theory

A
  • Once an initial critical mass of functioning nephronshave been removed:
  • Progression to End-Stage Renal Disease
  • INEVITABLE
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11
Q

Pathophysiologyof CKD / CRF diagram

A
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12
Q

increased tubular processing of proteins leads to which condition

A

tubulo intestitial nephritis

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13
Q

increased processing of proteins in the mesenchymal cells leads to

A

glomerulosclerosis

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14
Q

sings of progressive crf

A
  • Continuation of primary disease
  • Systemic / metabolic abnormalities
  • Increases in phosphorus, PTH, BP
  • Adaptive changes in surviving nephrons
  • Tubulo-interstitial injury
  • Intraglomerularhypertension (SNGFR)
  • Systemic hypertension
  • Renal 2ndhyper-PTH
  • Renal mineralization (Ca x P product)
  • UTI
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15
Q

Hypertension in CRF:Clinical Manifestations

A
  • Ocular
    • Blindness
    • Retinal detachment
    • Retinal hemorrhages
    • Retinal vascular toruosity
  • Cardiovascular
    • LV enlargement
    • Medial hypertrophy of arteries
    • Murmurs and gallops
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16
Q

discuss characteristics of stage 1 crf

A

non azotemic ckd

prevalence =7.1%

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17
Q

discuss stage 2 of crd

A

mild renal azotemia

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18
Q

discuss stage 3 crd

A

moderate renal azotemia

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19
Q

discuss stage 4 crd

A

severe renal azotemia

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20
Q

which crd stages are apparent

A

3 n 4

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21
Q

prognosis for cats and dogs with crd

A

Cats
Often live months to years
Dogs
Much less likely long term survival ( < 1 year? )

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22
Q

Treatment of CRF -Uremia

A
  • Make animal feel better
  • Reduce uremic lesions
  • Prevent (slow down) further loss of renal function
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23
Q

Management of CRF:General Principles

A

Search for reversible causes
Pyelonephritis
Obstruction (uroliths, neoplasia)
Hypercalcemia
Don’t pass judgementon animal until several days of conscientious fluid therapy for those with decompensatedCRF

24
Q

initial Conservative Medical Management

A

Dietary phosphorus restriction
Dietary protein restriction
Intestinal phosphate binders
H-2 receptor blockers

25
Q

secondary Conservative Medical Management for crd

A

Control of systemic hypertension
Control of renal 2ndhyper-PTH
Control of metabolic acidosis
ACE inhibition (w/ or w/o hypertension)
EPO

26
Q

discuss dietary phosphorus in crd

A
  • Phosphorus Restriction
  • Single most powerful treatment
  • Extends life of kidney
  • Extends life of patient (quality)
27
Q

discuss effects of Protein Restriction in crf

A
  • Uremia/Renal Disease is Progressive
  • Cachexiais a common problem in CKD/CRF
  • Effects of too little dietary protein?
  • Could it be protein malnutrition?
28
Q

how to solve protein problem in crd

A

If decrease in caloric intake occurs……….
Must increase % protein concentration
Otherwise, decreased protein reserves occurs

29
Q

Medical Management of CRF:Uremic Gastroenteritis

A

Plasma gastrinconcentrations are high in dogs/cats with CRF
Degree of hypergastrinemiacorrelates with severity of CRF
Potential manifestations:
Anorexia
Vomiting
GI bleeding

30
Q

Benefits of Dietary Pi Restriction

A
  • Canine Induced Renal Failure
    • Slows progression (Brown 1991)
  • Feline Induced Renal Failure
    • Decreased mineralization
    • Decreased fibrosis (Ross 1982)
31
Q

how Intestinal Phosphate Binders works

A

All work best when given with food or near time of food intake

32
Q

Most commonly used intestinal Pi binder in Vet Med

A

Aluminum Salts (Aluminum Hydroxide)

33
Q

advantages of Aluminum Salts (Aluminum Hydroxide)

A

Inexpensive
Good Pi-binding

34
Q

disadvantages of Aluminum Salts (Aluminum Hydroxide)

A
  • Constipation –common side effect
  • Largely abandoned in human medicine
    • Aluminum is toxic
    • Accumulates if kidneys are diseased
    • No known safe dose for humans with CKD
    • Good choice in vet med?
35
Q

discuss Calcium Carbonate phosphorus binding

A
  • 100 mg/kg divided with meals
  • Follow S-Pi and adjust dose
36
Q

disadvantages of calcium carbonate

A
  • Careful in patients receiving calcitriol(hypercalcemia)
  • Phosphorus binding = LESS than aluminum
37
Q

advantages of calcium acetate

A

Better phosphusbinder than calcium carbonate
PhosLo= 3x Pi binding
Less risk of hypercalcemia

38
Q

Chitosan-based supplement (shellfish exoskeleton)

A
  • Epakitin
  • 10% Calcium Carbonate
  • No taste aversion?
39
Q

PropietaryPump Delivery System to food

A
  • Renalzin(Bayer)
    • LantharenolCarbonate
    • Anti-oxidant effects
    • Approved as food additive (EU & Japan)
40
Q

SevelamerHCl(Renagel)

A
  • Does not contain Ca+2 or Al+3
  • 30-60 mg/kg/day divided and given with food
  • May cause GI adverse effects including constipation
  • At extremely high dosage may interfere with GI absorption of folic acid, vitamin D, and vitamin K
  • Expensive
41
Q

Lanthanum carbonate (Fosrenol®)

A
  • Potent intestinal phosphate binder
  • Similar to Al(OH)3; more potent than calcium carbonate & calcium acetate
  • Not absorbed from intestinal tract but trace amounts have been reported in liver & bone
  • Excreted in bile
  • No apparent toxicity
  • 375 to 3,000 mg per day in humans
  • Start at 10-40 mg/kg/day ?
42
Q

effects of Hormonal Replacement: Erythropoietin on dogs and cats

A
  • Resolution of anemia
  • Weight gain
  • Improved appetite
  • Improved haircoat
  • Increased alertness
  • Increased activity
43
Q

when should u consider giving erythropoitin

A
  • Consider in symptomatic dogs and cats with PCV < 20%
    • Starting dosage 100 U/kg SQ 3X per week
    • When PCV > 30% decrease to 2X per week
44
Q

how to monitor erythropoitin hormonal replacement s

A
  • Monitor PCV weekly using same technique (table top centrifuge or Coulter counter) every time
  • Target PCV range: 30 to 40%
  • Depending on severity of anemia may take 3 to 4 weeks for PCV to enter target range
45
Q

adverse side effects of erythropoitin hormonal replacements

A
  • Antibody formation
  • Vomiting
  • Seizures
  • Hypertension
  • Uveitis
  • Hypersensitivity-like mucocutaneousreaction
46
Q

discuss Antibody formation due to erythropoitin hormonal replacement

A
  • High risk of antibody formation
  • Occurs 30 to 160 days after starting treatment
  • Progressive decrease in PCV and marked increase in bone marrow M:E ratio while receiving EPO
  • Discontinue EPO if antibody formation suspected
  • Prolonged transfusion dependence may result
47
Q

discuss Calcitriol hormonal replacements

A
  • Enhances gastrointestinal absorption of calcium and corrects ionized hypocalcemia
  • Reduces PTH secretion by occupying calcitriolreceptors on parathyroid glands
48
Q

discuss use of calcitrol in crd

A
  • Used only after hyperphosphatemiacontrolled
  • (Ca Pi < 60-70)
  • Watch for hypercalcemia(especially with Ca+2containing Pi binders)
  • Rapidly lowers serum PTH concentration
49
Q

discuss dose for calcitrol

A
  • Extremely low dosage required: 2.5 to 3.5 ng/kg/day
  • Requires reformulation by compounding pharmacy
  • Can use “pulse dosing”
50
Q

discuss monitoring patients on acitrol

A
  • Monitoring patients on calcitriol
  • Clinical appearance may be unreliable
  • Follow serum PTH concentration
  • Long-term benefit to animal unknown
51
Q

discuss assessment of bp in patients with crd

A
  • Oscillometricor Doppler methodology acceptable in dogs
  • Doppler methodology more reliable in cats
52
Q

when do u decide to tx hypertension

A
  • BP consistently > 160 mm Hg
  • High BP and fundiclesions
    • Retinal hemorrhage
    • Vascular tortuosity
    • Retinal edema
    • Intra-retinal transudate
    • Retinal detachment
53
Q

Medical Management of CRF:Treatment of Hypertension

A
  • Dietary salt restriction
    • Commercial pet foods designed for CRF often also are sodium-restricted
  • Diuretics
    • Risk of dehydration and pre-renal azotemia greater with loop diuretics (e.g. furosemide) than with thiazides(e.g. hydrochlorothiazide
54
Q

drugs fopr mananging hypertention in crd

A
  • Amlodipine
    0.18 mg/kg in dogs or 0.625 to 1.25 mg per cat PO q24h
    Recheck BP one week after starting drug
  • Enalapril
    0.5 mg/kg q12h or q24h
    Effect on blood pressure may be modest
    May have other potentially beneficial effects on kidney
55
Q

indicative of a poor prognosis in crf

A
  • Severe intractable anemia
  • Advanced osteodystrophy
  • Inability to maintain fluid balance
  • Progressive azotemiadespite treatment
  • Progressive weight loss
  • Severe endstagerenal lesions on biopsy

small animal medicine (3 decks)

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