5 Laminitis and Founder in Horses

Which of the following best describes the relationship between laminitis and founder in horses?

The primary and secondary laminae in a normal equine foot are crucial for:

Considering the vascular supply to the equine digit, which statement is most accurate regarding blood flow to the laminae?

Historically, laminitis pathogenesis was attributed to a 'One Mechanism' theory. Current understanding emphasizes:

In Systemic Inflammatory Response Syndrome (SIRS)-associated laminitis, which of the following is considered a key mediator in the digit inflammation?

Metalloproteinase enzymes (MMPs), specifically MMP-2 and MMP-9, are implicated in laminitis pathogenesis due to their role in:

The Ischemia/Vascular theory of laminitis pathogenesis, supported by studies over the last 30 years, centers around:

Mechanical or traumatic laminitis differs from systemic disease-related laminitis primarily because it:

While hyperglycemia can occur in critically ill horses and have detrimental effects, experimentally, it is hyperinsulinemia that is strongly linked to the induction of laminitis. Why is this distinction critical?

Endocrinopathic laminitis, often associated with Equine Metabolic Syndrome (EMS) and PPID, is characterized by:

Which of the following scenarios would be LEAST likely to induce glucocorticoid-associated laminitis?

'Grass founder' is often linked to Metabolic Syndrome. What is the most probable underlying mechanism connecting lush pasture and laminitis in susceptible horses?

In cases of laminitis, 'rotation' of the coffin bone (P3) within the hoof capsule implies:

'Sinking' or vertical displacement of P3 in laminitis signifies:

Carbohydrate overload-induced laminitis is experimentally reproducible and involves:

Black walnut shavings are a known cause of laminitis. The mechanism is:

Systemic diseases like colitis and retained placenta are associated with laminitis due to:

Clinical signs of laminitis typically include lameness. An 'Obel 2' lameness grade is characterized by:

Toe pointing in a horse with suspected laminitis is a clinical sign indicating:

Sweating and tachycardia observed in a horse with laminitis are indicative of:

An increased digital pulse and warm hoof in a horse are clinical findings consistent with:

A ridge or depression at the coronary band in a horse's hoof is a clinical sign suggestive of:

Hoof testers in laminitis cases typically elicit a pain response when pressure is applied over the:

'Rings' in the hoof wall of a horse are often associated with:

Nerve blocks, specifically a palmar digital or abaxial sesamoid block, are used in laminitis diagnosis to:

Radiographs are NOT necessarily required to diagnose laminitis, but are crucial for:

Lateral radiographs in laminitis cases are specifically evaluated to assess:

Osteophyte formation and remodeling of the distal phalanx (P3) observed on radiographs indicate:

Radiographic 'lysis' of P3 in advanced laminitis signifies:

Treatment of laminitis is complex and lacks a single 'best' approach primarily because:

A primary principle in laminitis treatment is to address the underlying disease. This is crucial because:

Phenylbutazone is commonly used in laminitis management primarily for its:

While NSAIDs are a mainstay of laminitis pain management, opioids and alpha-2 agonists like detomidine are sometimes used, but with caution due to:

DMSO (dimethyl sulfoxide) is used in laminitis treatment based on its purported action as a:

Pentoxifylline, used in laminitis therapy, is a phosphodiesterase inhibitor believed to improve blood flow by:

Steroids are generally contraindicated in the treatment of laminitis primarily due to their potential to:

Reducing mechanical forces on the weakened laminae is a crucial aspect of laminitis management. This principle is addressed by:

Raising the heels in therapeutic shoeing for laminitis aims to:

A heart bar shoe is typically applied in the chronic phase of laminitis to:

Deep digital flexor (DDF) tenotomy is a surgical procedure considered in chronic, severe laminitis cases to:

Hoof wall resection surgery in laminitis is now considered 'fallen out of favor' primarily because:

Vasodilators like acepromazine and nitroglycerin are sometimes used in laminitis treatment based on the Ischemia/Vascular theory. Their primary mechanism of action is to:

In horses, what is the fundamental difference between laminitis and founder?

Considering the anatomical structure of the equine foot, what is the functional significance of the primary and secondary laminae?

How does blood flow to the laminae contribute to the pathogenesis and treatment of laminitis?

Why is the shift from the 'One Mechanism' theory to 'Many Factors' a significant advancement in understanding laminitis?

Why are PMNs (polymorphonuclear neutrophils) significant in the pathophysiology of laminitis associated with SIRS?

How do matrix metalloproteinases, specifically MMP-2 and MMP-9, contribute to the pathophysiology of laminitis?

How does the ischemia/vascular theory explain the pathogenesis of laminitis?

How does mechanical or traumatic laminitis differ from systemically-induced laminitis at the level of initial pathogenic events?

What is the primary significance of hyperinsulinemia in the pathogenesis of endocrinopathic laminitis as opposed to hyperglycemia?

How is endocrinopathic laminitis, often associated with Equine Metabolic Syndrome (EMS) and PPID, characterized?

What aspect of insulin dysregulation is thought to predispose horses to glucocorticoid-associated laminitis?

Why is identifying 'grass founder' as a manifestation of Metabolic Syndrome crucial for managing at-risk horses?

When assessing radiographs in a laminitic horse, what does the term 'rotation' of the coffin bone (P3) specifically imply?

What does 'sinking' of P3 in laminitis indicate about the severity and nature of the lamellar damage?

How does carbohydrate overload induce laminitis experimentally, and what is the underlying mechanism that connects these two events?

What is the current understanding of how black walnut shavings cause laminitis, and what makes this etiology unique?

How do systemic diseases like colitis and retained placenta increase the risk of laminitis, and what common pathway is involved?

What is the significance of toe pointing as a clinical sign in a horse suspected of having laminitis, and what does it indicate about the horse's discomfort?

What is the underlying physiological reason for the sweating and tachycardia observed in a horse experiencing laminitis?

Why is it clinically relevant to assess for a ridge or depression at the coronary band in a horse suspected of having laminitis?

What is the significance of pain elicited during hoof tester examination when pressure is applied over the toe region in a horse with suspected laminitis?

How and why do 'rings' in the hoof wall provide a historical record of laminitis or other metabolic disturbances?

How can nerve blocks aid in the diagnosis of laminitis, and what is the limitation of their use in determining the underlying cause?

If radiographs are not necessarily required to diagnose if a horse has laminitis, what critical information do radiographs supply?

Why is the use of lateral radiographs considered important in the evaluation of laminitis cases?

What do osteophyte formation and remodeling of the distal phalanx (P3) on radiographs tell you about the laminitis?

What is the significance of radiographic 'lysis' of P3 in advanced laminitis cases, and what does it suggest about the severity of the condition?

Given that laminitis treatment is complex and lacks a universally effective approach, what single principle is the most crucial in achieving a positive outcome?

While NSAIDs alleviate pain, what is one major limitation of NSAID use in laminitis cases?

What is the primary mechanism of action of dimethyl sulfoxide (DMSO) in laminitis treatment, and how does this action theoretically help?

What is the proposed mechanism by which pentoxifylline aids in the treatment of laminitis, and what specific property of blood does it aim to improve?

What is the primary biomechanical rationale for reducing mechanical forces on the weakened laminae in laminitis cases?

What is the biomechanical advantage of raising the heels in therapeutic shoeing for laminitis cases with regard to the deep digital flexor tendon?

Why is a heart bar shoe typically applied in the chronic phase of laminitis, and what specific structure of the foot does it aim to support?

In advanced, refractory laminitis what is the goal of performing a deep digital flexor (DDF) tenotomy?

While vasodilators like acepromazine and nitroglycerin can be used in laminitis, why is there concern about their efficacy?