Laminitis (Menzies-Gow) Flashcards
What is laminits?
- failure of attachement of epidermal cells of insensitive laminae (epidermal) to underlying basement membrane of sensitive laminae (dermal)
What 2 direction can the pedal bone move in?
Rotate or sink down
Risk factors for laminits
> sepsis and sysetmic inflammation
- GI disease, sick neumonia, septic metritis
endocrine disorders
- PPID and EMS
mechanical overload
- non-weight bearing lame for significant period of time (contralateral laminitis)
access to pasture
PDF for laminitis
- pony
- spring/summer (related to grass)
- female (maybe)
- ^ age
- obesity
- recent ^ BCS
- recent access to new grass
- ^ time since worming(? reason for link)
- insulin resistance
3 stage of laminitis?
- developmental
- lasts ~72hrs
- contact w/ trigger and breakdown of attachemnts
- NO CLINICAL SIGS - acute
- clinical signs seen - Resolution or progression to chronic laminitis
Main 4 aspects of pathogenesis?
- inflammation
- ECM degradation
- metabolic disease
- endothelial and vascular dysfunction > exact mechanism not elulcidated
How is inflammation involved in laminitis?
- minimal neutrohil infiltration histopathologially - role questioned
- lamellar inflammation definiely involved now
- ## hindgut fermentation of carbs in gut -> systemic inflam with only overt signs in the pony’s feet ? Inflam seen elsewhere in the body too
How is ECM degradation involved in laminitis?
- (ECM = structural proteins, proteoglycans, regulatory proteins, proteases, protease inhibitiros. Responsible for maintainance of structural support, remodelling, healing)
- previously thought MMPs fundamental - now shown not an initiating event (but is involved)
- now shown laminar separation = failre of adhesion molecules called hemidesmisomes (attach epidermal cells to basement membrane)
- somehow these are moe liekly to fail in the feet (inflam? hypoxia and reperfusion injury?)
How is metabolic disease linked to laminitis?
- greatest risk of laminitis assocaited with ‘metabolic phenotype’ (eg. obesity, insulin resistance)
- endothelial cell dysfunction caused by mediators from adipose tissues
- hypertension?
- may be exaccerabation of IR by increased carbs (grass intake) -> laminitis in summer/spring
> NB not all laminitis prone ponies are obese and not all obese ponies are laminitis
How are ascualr and endothelial cells indicate in lamintis?
- digital vasoconstriction and consequent laminar oedema
- venoconstriction d/t platelet activation and platelet neutrophil acitvation -> vasoactive mediator 5HT
- amines from hidgut fermentation of CHO are vasoactive
- IR in other species alters endothelial function -> pro-inflam condition -> platelet and leucocyte activation, ^ production ET1 and production of mediators of inflame and oxidant stress
What aret he aims of the workup?
- definitive dx
- determine cause
- prognosis of recovery and soundness?
How many legs are commonly affected in laminitis?
More than one (can be one, but very unlikely)
Clinical signs of laminitis
- 2+ limbs
- leaning on heels
- bounding digital pulses
- hoof wall may feel warm
- pain in hoof testers at the point of the frog
- palpable depression at the coronary band (extensor process of pedal bone should -> solid uncompressable area, otherwise indicates pedal bone has sunk. POOR PROG)
What further diagnostics can be carried out for lamintis?
- Imaging
- Endocrine tests
When would radiographs be indicated?
> concern P3 has moved - palpable softening at point of frog - depression at coronary band > if not improing * can be difficult, may need +- nerve blocks*
