Equine Pituitary Pars Intermedia Dysfunction - Paper Example

The Equine pituitary pars intermedia dysfunction (PPID) is one of the widely known disease infecting aged horses. In the last twenty years, the number of aged horses has increased significantly, and as a result, there has been an increase in the awareness of PPID among veterinary personnel (McGowan and Pinchbeck 2013, p. 72). The diagnostic testing and treatment of the disease have been expanded to improve the provision of safe and quality care to prevent potential fatalities. In this paper, the etiology and symptoms of PPID are explored in detail and its significance in the life of domesticated equine. Besides, this paper identifies the best care plan that is suitable for the treatment of the affected horses.

Etiology

PPID disease also known as the Equine Cushings Disease is a neurodegenerative malfunction of the hypothalamus that leads to the loss of dopaminergic inhibition of pars intermedia (McGowan and Pinchbeck 2013, p. 72). This affects the normal functioning of the endocrine or hormonal system of horses. The principal centers for the synthesis and release of hormones are the pituitary gland and hypothalamus regions of the brain that lies deep inside the skull of horses. The pituitary gland in equine is divided into three sections: the pars distalis (anterior pituitary), the pars intermedia (intermediate lobe), and the pars tuberalis (posterior pituitary). The pituitary gland produces hormones, which are mainly chemical messengers, that are then distributed around the horse body through the bloodstream to all the tissues to perform essential functions such as metabolism, lactation, growth, and reproduction. In healthy equine, these hormones are distributed in a fine balance to play an integral role in coordinating and maintaining these important body functions. This ensures the quinine body functions at optimum level (Klinkhamer, Menheere and Van Der Kolk 2011, p. 22).

When horses grow older, usually between fifteen to twenty-one years of age, the neurons in the hypothalamus that innervate and regulate the intermediate lobe progressively degenerate at a faster rate and hence synthesize low quantities of a nerve transmitter substance referred to as dopamine. Dopamine is an essential hormone required to regulate the secretions of hormones from pars intermedia section of the pituitary gland, which play an important role in the production and release of hormones (Peel, Flach, Routh, Bouts, and Rivers 2009, p.774). It is required to control the secretions of hormones such as adrenocorticotropin (ACTH). Therefore, this degeneration leads to the insufficient release of dopamine to pars intermedia, which causes in the process the intermediate lobe to become much more active and increase the synthesis and release of abnormally high levels of cortisol and ACTH hormones that ultimately result in the symptoms linked with the PPID.

As explained by Spelta (2015), the elevated release of ACTH from pars intermedia stimulates the adrenal glands to produce excessive cortisol hormone. The cortisol hormone along with ACTH give rise to the individual clinical signs of PPID, which after some time, the affected horses may develop pituitary tumors, usually referred to as adenomas that can compress adjacent structures resulting in neurological signs.

The disease was first discovered in 1932 and was identified as an advanced malfunction that affected aged horses usually above fifteen years old. Since then PPID has been researched and proper management practices devised to control its severity (Carmalt, 2017). It has been discovered that all light horse breeds are susceptible to the disease. Additionally, horses that are affected by Equine Metabolic Syndrome are usually at higher risk (McFarlane 2007, p.56). Once horses exhibit this malfunction, they develop a wide range of nonspecific clinical symptoms that become severe over time. It is characterized by persistent, long, curling hair coat, pendulous abdomen, and heightened risk of laminitis and epaxial muscle wastage. Over the last decade, considerable research to ascertain the etiology of PPID has been carried out (McFarlane 2007, p.56).The recent findings indicate the main cause of the disease is an aged- induced neurodegeneration of dopaminergic neurons located in the hypothalamus region of the brain. The findings by Cordero, McFarlane, Breshears, Miller, and Duckett (2012) though not substantially proven suggest that the disease is caused by oxidative stress. Once the dopamine inhibition capability is weakened, pars intermedia produce excessive ACTH that marks the beginning of the disease. The assessment of the exact initiating causative factor is often complicated because the clinical symptoms are mainly detected after a substantial amount of years has elapsed.

According to Durham, McGowan, Fey, Tamzali, van der Kolk (2014, p 219), the degeneration of dopaminergic neurons is largely caused by misfolding of a protein known as alpha-synuclein and oxidative stress, which has been noted in increasing prevalence in PPID horses (Durham et al.2014, p 219). The misfolding, characteristic poor development of the protein other than fold into the normal functional shape has been proven to be caused by oxidative stress. The dopaminergic neurons are mainly predisposed to oxidative damage since dopamine metabolism initiates free radicals that suppress the normal functioning of cells. These radicals are chemically molecular fragments without electrons that are quite harmful and destroy large molecules inside cells while attempting to attain a more stable configuration (Durham et al.2014, p 220). Other factors that cause dopaminergic degenerations include mitochondrial dysfunction and inflammation.

In a healthy pituitary gland, the pars distalis ensures that most ACTH hormones are synthesized with small quantities of ACTH from melanocyte-derived pro-opiomelanocortin (POMC) (Beech, Boston, McFarlane and Lindborg 2009, p. 717). The intermediate product synthesized by pars intermedia is a-melanocyte stimulating hormone (MSH), which is a metabolically active peptide involved in obesity and metabolism containing potent anti-inflammatory properties. The glucocorticoid negative feedback loop controls the production of corticotrophs in the pars distalis.

A region in the Pars intermedia known as melanotropes is responsible for the synthesis and secretion of the POMC peptides (Geor and Harris 2009, 52).This synthesis is influenced by dopamine inhibitory control that originates from the hypothalamus. The secretion of hormones in pituitary and hypothalamus are largely influenced by seasons and photoperiod length (Schreiber, Stewart and Kwessi 2012, p. 244). For instance, during winter and late summer, the months during which there is minimal day length, up-regulation of ACTH and MSH productions rise significantly. This rise is the survival mechanism of horses to elevate the storage of fats in preparation for harsh winters when there is an anticipated small amount of feeds. This similar mechanism is initiated in horses affected with PPID even though the regional fat deposition is not carried out in anticipation of winter periods.

The Clinical Symptoms

The major symptom of this disease is the formation of abnormal curling, long or wavy hair coat; a condition referred to as hirsutism. These symptoms become visible once the hormonal imbalance is prolonged (McFarlane, 2006). The apparent long hair coat in PPID horses is attributed to the persistence of hair follicles in the anagen stage. The follicles trapped in the anagen stage often become difficult to be shaded as evident in PPID affected equine or horses.

Laminitis is another major symptom of PPID. It is an inflammation of the hoof characterized by the release of the pulse. This condition is observed immediately a horse starts to experience abnormal too little, or too much foot lifting, a shortened stride, an increased heart rate, and a distorted hoof shape (Innera, Petersen, Desjardins, Steficek, and Rosser 2013, p. 214). The PPID-associated laminitis has been known historically to be caused by increased release of cortisol levels. However, recent research shows that laminitis pathogenesis has a strong association with concurrent hyperinsulinemia. The actual mechanisms of this association between the PPID and hyperinsulinemia have not been figured out, but it is a subject of ongoing research.

Other symptoms include lethargy, sweating abnormalities, and epaxial muscle wastage, polydipsia/polyuria, increased susceptibility to infection, a pendulous abdomen and poor wound healing (Nourian, Asplin, McGowan, Sillence, and Pollitt 2009, p. 672). Lethargy condition is observed when a horse decreases its alertness, become sluggish, exhibit low energy or experiences changes in mood. Sweating abnormalities is usually evident when a horse either produces no sweat at all or releases sweat in abnormally high quantities. Epaxial muscle wastage can be observed when a horse begins to lose weight. The excessive production of cortisol and ACTH hormones result in the production of dilute urine; a condition called polyuria or polydipsia. This is because ACTH hormones prevent water reabsorption in the kidneys into the bloodstream, leading to the release of large quantities of dilute urine. The PPID affected horses become more susceptible to other infections such as endoparasitism due to hormonal imbalance that suppresses the normal immunity of the body (Nourian et al. 2009, p. 672). As a result, non-healing wounds are formed that subject excessive pain to the affected horses. This disease is a lifelong chronic problem without a cure.

The Management Of PPID And The Best Care Plan To Use For The Affected Horse

The diagnosis given for the eighteen-year-old 16.2hh thoroughbred gelding proves beyond any reasonable doubt that the horse is affected by PPID. The presence of a non-healing wound on the hoof as well as notable weight loss, excessive sweating, polyuria and lethargy symptoms shows the horse needs immediate care and management. Therefore, an appropriate management practice that adopts the best care plan must be selected and implemented accordingly.

The predominantly used care plans include Roper, Logan, and Tierney Model, Orems Model and Ability Model. The first model, Roper, Logan, and Tierney offer the best care plan that is comprehensive unlike the other two. This is because it incorporates the assessment of different parameters that include maintaining a safe environment, communication, breathing, eating and drinking, elimination, washing, and dressing. It also incorporates controlling of temperature, mobilization, working, playing and expressing sexuality, sleeping and dying of a patient (Williams 2017, p. 18). Therefore, this model will be used to manage and provide care for the PPID affected horse presented.

After the horse is secluded and admitted in a secured environment, a thorough assessment of all the listed parameters given in this model must be carried out and recorded. The immediate intervention should focus on the administration of pergolide, a drug known to cause the release of dopamine to restore control of pars intermedia and hence lower the production of detrimental hormones (Mcfarlane 2011, 101). The horse condition is expected to improve significantly, as the visible clinical symptoms are regulated. However, it should be noted that this does not restore the natural release of dopamine, but only do so when this drug is still circulating in the bloodstream.

Since the horse exhibits advance symptoms, higher doses of pergolide within prescribed range should be administered alongside a serotonin antagonist, and cyproheptadine (Spelta and Axon 2012, p. 452). This drug has not been definitively prove...