Overview of Homeostatic Control

Discuss about the Journal of veterinary internal medicine.

This is a self controlling system that allows a stable biological system to be maintained in the form of a dynamic equilibrium, through series of inter related changes.

There are three components in a homeostatic system, namely the receptor, effectors and control. The control can be intrinsic (local control that work in local environments) and extrinsic control (through the actions of nervous system, endocrine system or neurohormonal actions) (d.umn.edu, 2018). The control can be through a system of positive and negative feedback mechanisms. The feedback system works in a manner that allows the maintenance of consistency in the system (Nayak, 2018). In the negative feedback, the action of the effectors causes a negative effect on the change, and thus the effect of the negative feedback system has suppressive action on the response. AN example of negative feedback system is the maintenance of body temperature (Cunningham, 2007; Aspinall & Cappello, 2015).

Variables controlled by the homeostatic system are: body temperature, levels of calcium, glucose, respiratory gases, oxygen levels, sodium, calcium potassium, pH on the plasma or blood; regulation of blood pressure; maintaining osmotic balance; cerebrospinal fluid composition and regulating gene expression and balance of energy metabolism (Nakamura, 2011).

	Hyperadrenocorticism Save Time On Research and Writing Hire a Pro to Write You a 100% Plagiarism-Free Paper. Get My Paper	Hypoadrenocorticism
What is	This is a disease that is identified by persistently elevated levels of cortisol in the system. It is also known as Cushing’s Syndrome, and affects older and geriatric dogs (Barbosa et al., 2016)	This disease is identified by a deficit in the production of adrenocorticotropic hormone, and low levels of cortisol in the blood.  This disease affects middle aged or young dogs most commonly (Lathlan & Thompson, 2018).
Deficient/Excess condition	Caused by excess production of cortisol	Caused by underproduction of cortisol
Aetiology	Excessive secretion of adrenocorticotropic hormones due to neuroendocrine tumours. It can also be due to adrenal carcinoma or adrenal hyperplasic syndrome (Raff et al., 2014). Due to this, the adrenocorticotropic hormone keeps on being produced regardless of the levels of cortisol in blood (Barbosa et al., 2016)	This can be caused because of atrophy or damage or destruction of the cortical region of the adrenal gland, because of which glucocorticoids and minerelocorticoids are produced insufficiently. The destruction of the cortical cells can e either immune mediated or due to fungal infection, neoplasia, trauma, amyloidosis or coagulopathy (Lathlan & Taylor, 2005)
Signs	Polyuria/Polydispsia; enlargement of the abdomen; Polyphagia; muscular weakness; lethargy; heat intolerance; alopecia; skin becomes thin and are prone to bruises and striation; skin hyperpigmentation; Calcinosis; atrophy of testis; facial paralysis; pyoderma; anestrus sebborhea and Pseudomyotonia (Cunningham, 2007).	Fluctuating levels of chlorine, sodium and potassium ions; persistent gastroenteritis; hypochloremia; hyperkalemia; hypoatremia; bradycardia; renal dysfunction; collapse of circulatory system; low blood pressure; dehydration; weakness; anorexia; diarrhea; low blood glucose levels; loss of weight and hyperpigmentation of dermis (Klein & Peterson, 2010).
Diagnosis	Adrenocorticotropic stimulation tests; measurement of Creatinine to cortisol ratio in the urine; intravenous and oral test of low and high dose dexamethasone suppression; analysis of the concentration of adrenocorticotropic hormone in the plasma; Complete count of blood. Diagnostic imaging techniques like thoracic and abdominal radiograph, ultrasound of abdomen, computerized tomographic test or magnetic resonance imaging test of the brain (Barbosa et al., 2016).	Adrenocorticotropic stimulation test; analyzing medical history, clinical signs and abnormalities in laboratory tests; radiograph of thoracic region; ultrasound of the abdomen and electrocardiogram test (Adler et al., 2016).
Treatment	Medical treatment can include administration of trilostane, mitotane, I-deprenyl and ketocon zole. Surgical treatment can also be used for removing the tumours in adrenal or pituitary glands (Barbosa et al., 2016).	This disease requires emergency medical assistance, where intravenous drip of saline should be administered. For shock, dexamethasone sodium phosphate or pednisolone sodium succinate is needed.. Also, replacement therapy for minerelocorticoids should be considered (Lathlan & Thompson, 2018).
Whether common in canine/feline/both	This is more common in Canines	Common in canines

	Hypercalcemia	Hypocalcemia
What is:	This disease is characterized by elevated levels of serum calcium or ionized calcium in blood (de Brito et al., 2017).	In this disease, the levels of calcium in the blood become very low (Quader, 2015).
Deficiency/Excessive conditions	Excess calcium concentration in blood	Deficient calcium concentration in blood
Aetiology:	Apocrine gland adenocarcinoma; Acromegaly; lymphoma; multiple myeloma; skeletal lesions; neoplasia of the bone or hyperparathyroidism. The condition is caused when excess calcium is released from the bones into the blood, absorption of excess calcium in the gastrointestinal tract or increase uptake/decreased excretion of calcium by kidneys. Over secretion can be due to over activity of thyroid, cancer, dehydration or even some medications (de Brito et al., 2017)	The disease is caused due to inadequate production of vitamin D, hypoparathyroidism or hormonal resistance. Such condition can be due to eclamsia, puerperal tetany, enema toxicity, rickets, and blood transfusions (Quader, 2015).
Signs:	Excess thirst and urination; upset stomach; nausea; vomiting; constipation; weakness of muscles; depression; cardiac arrhythmia or palpitations (Adam et al., 2016).	Encephalopathy; muscular cramps; hyperflexia; laryngiospasm; seizures (Mittendorf et al., 2004).
Diagnosis	The disease can be diagnosed on the basis of high levels of calcium, low levels of phosphorus of the blood; azotemia; low specific gravity if urine. Other tests include: ultrasonography; explorative surgery and measurement of serum parathyroid hormone (Adam et al., 2016).	Diagnosis can be done by estimating the levels of phosphate, parathyroid hormone, phosphate, alkaline phosphatase, vitamin d and calcium ion in blood and cyclic Adenosine monophosphate and phosphate in the urine (Refsal et al., 2001).
Treatment	Administration of glucocorticoids, diuretics, mithramycin, calcitonin and bisphosphonate. Intravenous fluid replacement therapy; and also surgical removal of the thyroid gland (Adam et al., 2016).	Intravenous administration of gluconate, oral administration of calcium and vitamin D (Refsal et al., 2001).
Whether common in canine/feline/both	Common in canine	Common in both

	Hyperthyroidism	Hypothyroidism
What is	This disease is characterized by the over activity of thyroid gland causing elevated levels of the thyroid hormones. It is also known as Grave’s disease (Daminet & Hill, 2017).	This disease is characterized by the underproduction of thyroid hormones by a less active thyroid gland (Kent et al., 2016).
Deficiency/Excessive conditions	Excess thyroid hormone	Deficient thyroid production
Aetiology	The disease can be caused because of over activity or enlargement of the gland thereby producing excess thyroid hormones. The enlargement can be due to malignant or non-malignant tumours in the thyroid gland Daminet & Hill, 2017).	This can be caused by the idiopathic atrophy (due to the reduction of thyroid parenchyma cells or lymphocytic thyroiditis (due to damaged thyroid follicles) of the thyroid. (Kent et al., 2016).
Signs	Loss of weight; increase in thirst, appetite and urinary flow; diarrhea; vomiting; hyperactive disorders; the fur coat appears unkempt, greasy or matted; restlessness or aggressiveness; elevated rate of heartbeats; weakness; breathing difficulties and even depression Daminet & Hill, 2017).	Fall of hair/fur; lethargy; weakness; slow beating of heart; obesity and lowering of temperature of body (Kent et al., 2016; Klein & Danzi, 2016).
Diagnosis	Diagnosis can be done by checking the thyroid gland for enlargements; monitoring heart rate and blood pressure; analysis of the levels of thyroid hormone and monitoring kidney and cardiac functions Daminet & Hill, 2017; Volckaert et al., 2016).	Analysis of the levels of thyroxin; stimulation tests for thyroid stimulating hormone and Thyrotropin releasing hormone; ultrasonography and Scintigraphy of thyroid and equilibrium dialysis test (Peterson, 2015).
Treatment	Iodine therapy; dietary therapy (restricting iodine intake in diet); surgery (removal of the gland); medications (like anti thyroid medicine) Daminet & Hill, 2017; Volckaert et al., 2016)	Oral levothyroxine and Intravenous levothyroxine. Regular follow-ups are needed for long term care (Peterson, 2015).
Whether common in canine/feline/both	Common in feline	Common in canine

Diabetes Mellitus is a metabolic disease in which the blood glucose levels becomes elevated that consequently affects the metabolism in the body. The disease has 2 distinct types: Type 1 and type 2. Type 1 diabetes mellitus is caused due to the underproduction of insulin while type 2 diabetes is due to a resistance to the hormone by the cells and tissues of the body (Vetmed.wsu.edu, 2018).

The disease can be caused due to the destruction of the beta cells of the pancreas by autoimmune action, or when the cells of the body stops responding to insulin (known as insulin resistance). The disease can be caused due to obesity, high blood pressure, genetic predisposition or family history; ethnic background; injury to pancreas; autoimmune disease; high levels of cholesterol in blood and pregnancy (gestational diabetes). Common symptoms include: frequent urination; dry mouth; increased appetite and thirst; weight loss; weakness; wounds take longer to heal; dry skin; neuropathy and infections. Treatment for diabetes includes change in diet; administration of insulin and concurrent treatment of any associated diseases (if any). The treatment is long term (Gilor et al., 2016; Öhlund et al., 2017; Davidson, 2015).

Hyperadrenocorticism: Causes, Symptoms, Diagnosis, and Treatment

Diabetes mellitus is different from diabetes insipidus, which is a disease caused due to a deficient secretion of the hormone Arginine Vasopressin or when the collecting tubules or distal tubules of nephron are unable to respond to the hormone (Rossi & Ross, 2018).

References:

Adam, Z., Starý, K., Kubinyi, J., Zají?ková, K., ?ehák, Z., Koukalová, R., … & ?ermáková, Z. (2016). Hypercalcemia, symptoms, differential diagnostics and treatment, or importance of calcium investigation. Vnitrni lekarstvi, 62(5), 370-383.

Adler, J. A., Drobatz, K. J., & Hess, R. S. (2007). Abnormalities of serum electrolyte concentrations in dogs with hypoadrenocorticism. Journal of veterinary internal medicine, 21(6), 1168-1173. DOI: 0.1111/j.1939-1676.2007.tb01933.x

Aspinall, V., & Cappello, M. (2015). Introduction to Veterinary Anatomy and Physiology Textbook-E-Book. Elsevier Health Sciences. Available at: https://books.google.co.in/books?hl=en&lr=&id=Iti4BwAAQBAJ&oi=fnd&pg=PP1&dq=Introduction+to+Veterinary+Anatomy+and+Physiology+Textbook-E-Book&ots=8WmS4RIcio&sig=U1l2cH_24rFxj5l0fJlmpiLUn9E#v=onepage&q=Introduction%20to%20Veterinary%20Anatomy%20and%20Physiology%20Textbook-E-Book&f=false

Barbosa, Y. D. S., Rodrigues, D. D. A., da Silva, N. C. B., Silva, F. L., da Silva, C. R. A., & Sousa, J. M. (2016). Hyperadrenocorticism in a dog: case report. PUBVET, 10(6), 460-465.

Cunningham, J. G., & Klein, B. G. (2007). Veterinary physiology. Missouri: Saunders Elsevier. Available at: https://sutlib2.sut.ac.th/sut_contents/H111503.pdf

D.umn.edu. (2018). Homeostatic Control Systems. D.umn.edu. Retrieved 15 March 2018, from https://www.d.umn.edu/~jkeener/hlth2040-1-su2012/pwreadings/pdf/1-3.pdf

Daminet, S., & Hill, K. (2017). Feline Hyperthyroidism. Chronic Disease Management for Small Animals, p 153.Available at: https://books.google.co.in/books?hl=en&lr=&id=GEk3DwAAQBAJ&oi=fnd&pg=PA153&dq=Feline+Hyperthyroidism+Daminet+Hill&ots=BBo80CvzqV&sig=ACY6kWxXCVegLidKfZEPSIfMNyA#v=onepage&q=Feline%20Hyperthyroidism%20Daminet%20Hill&f=false

Davison, L. J. (2015). Diabetes mellitus and pancreatitis–cause or effect?. Journal of Small Animal Practice, 56(1), 50-59.

de Brito, G. J., Schenck, P. A., & Chew, D. J. (2017). A Quick Reference on Hypercalcemia. The Veterinary clinics of North America. Small animal practice, 47(2), 241.

Gilor, C., Niessen, S. J. M., Furrow, E., & DiBartola, S. P. (2016). What’s in a name? Classification of diabetes mellitus in veterinary medicine and why it matters. Journal of veterinary internal medicine, 30(4), 927-940.

Kent, A., Constantino-Casas, F., & Herrtage, M. E. (2016). Naturally occurring acquired primary hypothyroidism in a cat due to lymphocytic thyroiditis. Veterinary Record Case Reports, 4(1), e000282.

Klein, I., & Danzi, S. (2016). Thyroid disease and the heart. Current problems in cardiology, 41(2), 65-92.

Klein, S. C., & Peterson, M. E. (2010). Canine hypoadrenocorticism: part I. The Canadian Veterinary Journal, 51(1), 63.

Lathan, P., & Thompson, A. L. (2018). Management of hypoadrenocorticism (Addison’s disease) in dogs. Veterinary Medicine: Research and Reports, 9, 1-10.

Lathan, P., & Tyler, V. J. (2005). Canine hypoadrenocorticism: pathogenesis and clinical features. Compendium on continuing education for the practicing veterinarian. Available at: https://www.vetfolio.com/internal-medicine/canine-hypoadrenocorticism-pathogenesis-and-clinical-features

Mittendorf, E. A., Merlino, J. I., & McHenry, C. R. (2004). Post-Parathyroidectomy Hypocalcemia: Incidence, Risk Factors, and Management/DISCUSSION. The American surgeon, 70(2), 114.

Nakamura, K. (2011). Central circuitries for body temperature regulation and fever. American journal of Physiology-Regulatory, integrative and comparative Physiology, 301(5), R1207-R1228.

Nayak, P. (2018). Homeostasis and Control System – physiologyforall. Sites.google.com. Retrieved 17 March 2018, from https://sites.google.com/site/physiologyforall/home/physiology/general-physiology/homeostasis-and-control-system

Öhlund, M., Egenvall, A., Fall, T., Hansson?Hamlin, H., Röcklinsberg, H., & Holst, B. S. (2017). Environmental risk factors for diabetes mellitus in cats. Journal of veterinary internal medicine, 31(1), 29-35.

Peterson, M. E. (2015). Primary goitrous hypothyroidism in a young adult domestic longhair cat: diagnosis and treatment monitoring. Journal of Feline Medicine and Surgery Open Reports, 1(2), 2055116915615153.

Quader, M. N. (2015). Investigation of Clinical Hypocalcaemia in Cattle and Goats at the selected Veterinary Hospitals in Bangladesh and India. Chittagong Veterinary and Animal Sciences University Khulshi, Chittagong-4225, Bangladesh.

Raff, H., Sharma, S., & Nieman, L. (2014). Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing’s Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia. Comprehensive Physiology, 739-769. https://dx.doi.org/10.1002/cphy.c130035

Refsal, K. R., Provencher-Bolliger, A. L., Graham, P. A., Cert, V. R., & Nachreiner, R. F. (2001). Update on the diagnosis and treatment of disorders of calcium regulation. Veterinary Clinics: Small Animal Practice, 31(5), 1043-1062.

Rossi, T., & Ross, L. (2018). VetFolio. Vetfolio.com. Retrieved 17 March 2018, from https://www.vetfolio.com/internal-medicine/diabetes-insipidus

Vetmed.wsu.edu. (2018). Diabetes Mellitus. Vetmed.wsu.edu. Retrieved 17 March 2018, from https://www.vetmed.wsu.edu/outreach/Pet-Health-Topics/categories/diseases/diabetes-mellitus

Volckaert, V., Vandermeulen, E., Daminet, S., Saunders, J., & Peremans, K. (2016). Hyperthyroidism in cats, part II: scintigraphic diagnosis and radioiodine treatment. Vlaams Diergeneeskundig Tijdschrift, 85(5), 265-273.