crf Flashcards
(56 cards)
1
Q
between cats and dogs,in which is renal dz common
A
cats
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)
3
Q
% of geriatric dogs affected by crf
A
CRF may affect 0.5 to 1.0% of the geriatric canine population
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)
5
Q
% of geriatric cats affected by crf
A
CRF may affect 1.0 to 3.0% of the geriatric feline population
6
Q
Clinical History in CRFF
A
- they are non specific
Polyuria/ polydipsia(common)
- Vomiting (dogs)
- Inappetance/ Anorexia
- Weight loss
- Lethargy
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)
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
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)
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
11
Q
Pathophysiologyof CKD / CRF diagram
A
12
Q
increased tubular processing of proteins leads to which condition
A
tubulo intestitial nephritis
13
Q
increased processing of proteins in the mesenchymal cells leads to
A
glomerulosclerosis
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
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
16
Q
discuss characteristics of stage 1 crf
A
non azotemic ckd
prevalence =7.1%
17
Q
discuss stage 2 of crd
A
mild renal azotemia
18
Q
discuss stage 3 crd
A
moderate renal azotemia
19
Q
discuss stage 4 crd
A
severe renal azotemia
20
Q
which crd stages are apparent
A
3 n 4
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? )
22
Q
Treatment of CRF -Uremia
A
- Make animal feel better
- Reduce uremic lesions
- Prevent (slow down) further loss of renal function
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
secondary Conservative Medical Management for crd
Control of systemic hypertension
Control of renal 2ndhyper-PTH
Control of metabolic acidosis
ACE inhibition (w/ or w/o hypertension)
EPO
26
discuss dietary phosphorus in crd
* Phosphorus Restriction
* Single most powerful treatment
* Extends life of kidney
* Extends life of patient (quality)
27
discuss effects of Protein Restriction in crf
* Uremia/Renal Disease is Progressive
* Cachexiais a common problem in CKD/CRF
* Effects of too little dietary protein?
* Could it be protein malnutrition?
28
how to solve protein problem in crd
If decrease in caloric intake occurs……….
Must increase % protein concentration
Otherwise, decreased protein reserves occurs
29
Medical Management of CRF:Uremic Gastroenteritis
Plasma gastrinconcentrations are high in dogs/cats with CRF
Degree of hypergastrinemiacorrelates with severity of CRF
Potential manifestations:
Anorexia
Vomiting
GI bleeding
30
Benefits of Dietary Pi Restriction
* Canine Induced Renal Failure
* Slows progression (Brown 1991)
* Feline Induced Renal Failure
* Decreased mineralization
* Decreased fibrosis (Ross 1982)
31
how Intestinal Phosphate Binders works
All work best when given with food or near time of food intake
32
Most commonly used intestinal Pi binder in Vet Med
Aluminum Salts (Aluminum Hydroxide)
33
advantages of Aluminum Salts (Aluminum Hydroxide)
Inexpensive
Good Pi-binding
34
disadvantages of Aluminum Salts (Aluminum Hydroxide)
* 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
discuss Calcium Carbonate phosphorus binding
* 100 mg/kg divided with meals
* Follow S-Pi and adjust dose
36
disadvantages of calcium carbonate
* Careful in patients receiving calcitriol(hypercalcemia)
* Phosphorus binding = LESS than aluminum
37
advantages of calcium acetate
Better phosphusbinder than calcium carbonate
PhosLo= 3x Pi binding
Less risk of hypercalcemia
38
Chitosan-based supplement (shellfish exoskeleton)
* Epakitin
* 10% Calcium Carbonate
* No taste aversion?
39
PropietaryPump Delivery System to food
* **Renalzin(Bayer)**
* LantharenolCarbonate
* Anti-oxidant effects
* Approved as food additive (EU & Japan)
40
SevelamerHCl(Renagel)
* 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
Lanthanum carbonate (Fosrenol®)
* 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
effects of Hormonal Replacement: Erythropoietin on dogs and cats
* Resolution of anemia
* Weight gain
* Improved appetite
* Improved haircoat
* Increased alertness
* Increased activity
43
when should u consider giving erythropoitin
* **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
how to monitor erythropoitin hormonal replacement s
* 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
adverse side effects of erythropoitin hormonal replacements
* Antibody formation
* Vomiting
* Seizures
* Hypertension
* Uveitis
* Hypersensitivity-like mucocutaneousreaction
46
discuss Antibody formation due to erythropoitin hormonal replacement
* 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
discuss Calcitriol hormonal replacements
* Enhances gastrointestinal absorption of calcium and corrects ionized hypocalcemia
* **Reduces PTH secretion by occupying calcitriolreceptors on parathyroid glands**
48
discuss use of calcitrol in crd
* **Used only after hyperphosphatemiacontrolled**
* (Ca Pi \< 60-70)
* Watch for hypercalcemia(especially with Ca+2containing Pi binders)
* **Rapidly lowers serum PTH concentration**
49
discuss dose for calcitrol
* Extremely low dosage required: 2.5 to 3.5 ng/kg/day
* Requires reformulation by compounding pharmacy
* Can use “pulse dosing”
50
discuss monitoring patients on acitrol
* **Monitoring patients on calcitriol**
* Clinical appearance may be unreliable
* Follow serum PTH concentration
* **Long-term benefit to animal unknown**
51
discuss assessment of bp in patients with crd
* Oscillometricor Doppler methodology acceptable in dogs
* Doppler methodology more reliable in cats
52
when do u decide to tx hypertension
* **BP consistently \> 160 mm Hg**
* **High BP and fundiclesions**
* Retinal hemorrhage
* Vascular tortuosity
* Retinal edema
* Intra-retinal transudate
* Retinal detachment
53
Medical Management of CRF:**Treatment of Hypertension**
* **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
drugs fopr mananging hypertention in crd
* **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
indicative of a poor prognosis in crf
* **Severe intractable anemia**
* Advanced osteodystrophy
* **Inability to maintain fluid balance**
* Progressive azotemiadespite treatment
* **Progressive weight loss**
* Severe endstagerenal lesions on biopsy
56
