59.HD pathogenesis

Question 1

define hip dysplasi

Answer 1

DEVELOPMENTAL (not congenital) condition that is multifactorial (under the influence of many factors mostly complex genetic and environmental influences) that leads to joint laxity and subsequent inflammation and osteoarthritis

Question 2

earliest age that dysplastic hips can be observed

Answer 2

hips are normal at birth, HD is a developmental disease earliest changes seen at 30 days (edematous ligament of the head of the femur)first radiographic signs at 7 weeks (sublux and poor development of cranial ace tabular rim)

Question 3

how do gluteals and adductor magnus counteract each other during weight bearing

Answer 3

deep and middle gluteals originate on ilial wing and insert on greater trochanter; f(x) ABduction and internal rotationadductor magnus originates on caudal ischiatic arch and inserts onto linea aspera of femur; f(x) ADDuction and external rotation

Question 4

T/Fdue to muscles, it is speculated that subluxation of femoral head occurs during swing phase and upon foot strike the pull of gluteals reduces the head of femur back into acetabulum

Answer 4

TRUEswing phase subluxates (rectus femoris, iliopsoas, sartorious)foot strike reduction (gluteals, adductors)will produce characteristic cartilage erosions (CATASTROPHIC REDUCTION maybe rather than catastrophic subluxation)

Question 5

two destructive events accompany functional subluxation

Answer 5

1. forces cross joint INCREASEbut2. area over which the forces are transmitted DECREASE

Question 6

what is quantitative trait loci

Answer 6

QTL–region on chromosome that contains genes or a group of genes responsible for PHENOTYPIC expression of a quantifiable trait (ie. hip dysplasia)Chromosome CFA03 for acetabular OA formation in Portugese Water Dogs

Question 7

what is the primary risk factor for the development of coxofemoral OA in all breeds studied

Answer 7

Distraction index (normal < 0.3) as a marker for joint laxity

Question 8

3 metric estimations for hip laxity

Answer 8

1. Norberg angle ( >105 degrees)2. Penn Hip (< 0.3)3. Femoral Head coverage (> 50%)

Question 9

joint fluid, muscle mass and hormones on the involvement of HD pathogenesis

Answer 9

1. joint fluid—suggests that dogs with laxity have more fluid (unknown if a primary or secondary mx)2. muscle mass–dogs with incr mass decr risk HD (greyhound) and vice versa with GSD 3. Hormones–estrogen, relaxin increased laxity4.

Question 10

weight/growth, nutrition and environment on the involvement of HD pathogenesis

Answer 10

1. wt/growth: fed ad lib at risk HD and had earlier progression of OA; caloric restriction 25% decr risk HD and OA 2. nutrition: dietary EXCESS Ca, vit D may delay endochondral ossification, high protein/CHO quality have not been fully validated theories3. environment: restricted diets; polysulfated GAG IM injections 6-8 weeks old decr risk HD

Question 11

T/Fpuppies delivered by Csection and raised had decrease risk HD

Answer 11

true

Question 12

percentage of dogs referred for hip dysplasia that have CCL injury

Answer 12

32% of dogs referred for HD have CCL injury

Question 13

three PE tests to eval for hip laxity

Answer 13

BardenBartlowOrtolani**can have FN! need to have combined diagnostic screening

Question 14

radiographic evidence of hip OA

Answer 14

1. femoral periarticular osteophyte formation2. subchondral sclerosis of craniodorsal acetabulum3. osteophytes on cr and cd acetabular margin4. joint remodeling5. joint incongruency

Question 15

direct comparison of OFA and Penn Hip

Answer 15

52% OFA excellent84% OFA good94% OFA fairhad DI>0.3

Question 16

T/F Cohort of labs, lean dogs live 1.8 years longer and required pain mgmt 3 years later compared to overweight dogs

Answer 16

TRUE

Question 17

two principal strategies used to control/prevent complex trait like HD

Answer 17

1. optimize selective breeding (genetic control)2. Prevent, Delay, or mitigate the gene expression