Laminitis - equine Flashcards
1
Q
What is laminitis characterised by?
A
failure of attachment of epidermal cells of the epidermal (insensitive) laminae to the underlying basement membrane of the dermal (sensitive) laminae
2
Q
Risk factors - laminitis
A
- sepsis and systemic inflammation (GIT disease, pneumonia, septic metritis)
- endocrine diseases (PPID and EMS)
- Mechanical overload (if one severely lame non weight-bearing limb, weight transferred to another)
- access to pasture
- pony > horses
- spring and summer
- female
- increasing age
- obesity
- recent increase in body weight
- recent new access to grass
- increased time since worming (but not directly related to parturition)
- insulin resistance (IR)
3
Q
3 stages of laminitis
A
- DEVELOPMENTAL: contact with trigger, lasts up to 72 hours, no overt signs
- ACUTE: see CS, lasts a few days or else –> chronic
- RESOLUTION or CHRONIC: exact cascade of events and interactions b/w these processes yet to be elucidated
4
Q
What are the 4 main pathogenesis categories of laminitis?
A
- inflammation
- ECM degradation
- metabolic disease
- endothelial and vascular dysfunction
- cascade and interactions of factors yet to be elucidated
5
Q
Outline role of inflammation
A
- previously questioned
- systemic inflammatory response that accompanies hindgut carbohydrate overload somehow initiates lamellar inflammatory events
6
Q
Outline role of ECM degradation and laminitis pathogenesis
A
- MMP activation does occur, not an initiating event
- laminar separation may occur following a failure of epithelial adhesion molecules (hemidesmosomes)
- dysregulation of cell adhesion most likely caused by inflammatory and/or hypoxic cellular injury
7
Q
Outline metabolic diseases in pathogenesis of laminitis
A
- greatest risk have metabolic phenotype (obesity and IR)
- similar to human metabolic syndrome (HMS)
- summer pasture appears to produce metabolic responses in laminitis prone ponies leading to expression of this at risk metabolic phenotype
- strong positive relationship b/w pasture NSC content and circulating insulin concentrations
- increased CHO consumption exacerbates IR In horses
- feeding a fructan-type CHO produces an exaggerated insulin response in laminitis prone ponies
8
Q
Outline vascular and endothelial dysfunction
A
- digital venoconstriction (early)
- consequent laminar oedema (early)
- venoconstriction d/t platelet activation and platelet-neutrophil activation –> release of vasoactive mediator 5-HT
- amines from hindgut fermentation of CHO are vasoactive
- IR in other spp alters endothelial function (proinflammatory condition, platelet and leukocyte activation, increased ET1 and production of mediators of inflammation and oxdant stress)
- digital vascular haemodynamic alterations (d/t inflammation, platelet activiation, action of vasoactive amines from GIT) –> lamellar injury
9
Q
Aims in approach to suspect case
A
- make definitive diagnosis
- determine underlying cause
- determine if likely to recover the expected level of soundness
10
Q
Dx - laminitis
A
- CS (lameness affecting 2+ limbs, characteristic stance of leaning back on heels, bounding digital pulses, increased hoof wall temperature, pain on hoof tester pressure at point of frog, palpable depression of coronary band)
+/- radiography (1st presentation - if concerned P3 moved, later - if CS not improving)
+/- enodcrine tests
11
Q
What might indicate P3 has moved? 2
A
- depression at coronary band
- softening of sole at point of hoof
12
Q
What radiographs need to be taken for suspect laminitis?
A
- lateromedial
- ensure good foot preparation
- put markers on feet (one on dorsal hoof wall starting at coronary band and one at point of bone)
- assess pedal bone rotation and founder distance (sinking)
13
Q
Which endocrine diseases might you want to r/o with laminitis?
A
- PPID
- EMS
14
Q
Dx tests - PPID
A
- CS
- basal ACTH (seasonally adjusted reference range)
- Dex suppression test (not autumn)
- TRH suppression test
15
Q
Dx - EMS
A
- Hx
- CS
- Demonstration of IR (fasting insulin and glucose, dynamic test)
