Essay on Course Notes

Submitted By waffles772
Words: 3805
Pages: 16

Ch9 laminitis * Laminae- attachment hoof wall and p3 * Laminitis- inflamatory process within laminae * Opposite pg 142 normal anatomy * 3 stages development: developmental, acute, acute chronic * laminitis- carbobhydrate overload, depending on type of carb quicker onset etc grain corn especially * get a change in bacteria of the gut, gram negatives are ecoli, they stain red, gram positive stains blue * past small intestine, in colon * bacteria normally there to help digest cellulose, help in hay digestions * in carb overlaod, not digested in stomach and small intesetine, bacteria proliferate and bloom in hind gut, back there bc digested so many of them cant all be digested * cell wall contains endotoxin- strong vascular toxin- irritates an inflames blood vessels * powerful vascular toxin causes swelling of small arteriols and venuls of capillaries of laminae- results in loss of blood supply to laminae, tissues die * weakening of attachment in front of foot, deep digital pulls in down and rearward till tip of bone protrudes through soul of the foot * developmental stage treatment- anti inflamatories, minize grain overalod w mineral oil, laxatives, preventative- put in ice * early acute stage- ansty in front feet, increased pulse, treatment the same w acute stage * if survive acute stage and don’t lose hoof wall enter chronic stage- permanent damage such a rotation or sinking of p3 can be salvaged but wont ever be the same * carb overload from grass, * prob in hind gut and gram negative bloom, when more carbs in hindgut then can handle * a gallon of grain is al a horse can handle wout possibility of carbs spilling into hindgut * other than carbs, gram neg bacteria and endotoxins * other then carbs , grass, cold water intake when hot, septosemia, concussive impact from hard work on hard surface, occasionally hormonal change in estrous cycle, increased temp from infection, pharmically induced laminitis- main culprit cortical steroids * concusion on hard surface usuaslly milder, w treatment good chance of successful outcome * anatomy of laminae- approx. 600 pairs of laminae that connect w insensitive laminae, endtoxin becomes vasucalr poison, congestion of circulation, laminae break down, degree of severity depends onhow many laminae involved * no such thing as mild case, can g from grade 1 to 4 very quickly, any indication – parked out, increased pulse, anxious look in eyes, warm feet * foundered horses foot warm all the way around, doesn’t get relief from vascular shunt * ice for minimum of 24 hours, this eliminates pressure in capailarries and dissolving the breakdown of as many laminae as possible * if no vascular shunt that allows blood to bypass foot, feet would freeze #4 totally false * septosemia- septic infection in the blood, bloodp oisoning, can casue it- impregnant mare who hasn’t passed palcenta- cooks in uterus and starts digesting all that septic fluid is absorbed in gut causes laminitis * 148 or 6 shows thermograph, p3 to anterior hoof wall should be parallel * chronic stage have to eliminate possible prombels : navicular, sole absess, ring bone, white line disease * principles: prevent absorbtion of endotoxin, aspirin as anticoagulant to stop clotting in feet, analgesics and nsaids are your best friends * frog support after ice or during ice, tape on w elasticon tape, stirofoam * trimming off toe, 4 point trim to supply 4 points of pressure * stand in sand, in creek, * chronic stage shoeing- hospital plate- frog usport such as heart bar- principles to ease breakover, shoes on backwards (open toed egg bar)
-elevate heels, takes pressure off depp digitial flexor * determine when disease will end, prognonsis for laminitis- guarded in all cases- don’t know where its going to end * haught- puts in ice and on nsaids, ulcergaurd if in bute, equiox- not as good painkiller