Front: What is the endocrine system composed of?
Back: Groups of tissues that form organs
Front: How do endocrine tissues release hormones?
Back: They are ductless and release hormones directly into circulation
Front: What is a hormone?
Back: A signaling molecule
Front: What are the three types of hormones?
Back: Protein hormones, steroid hormones, modified amino acid hormones
Front: How do hormones function?
Back: Travel to distant targets, interact with receptors, and create effects
Front: What do hormones control?
Back: Biological processes and most tissues
Front: Is endocrine dysfunction common?
Back: Yes
Front: Where are protein hormones produced?
Back: In endocrine tissues via gene transcription
Front: What triggers protein hormone release?
Back: Specific signals (e.g., insulin secretion with increased glucose)
Front: Are protein hormones stored in large amounts?
Back: Yes, for quick release
Front: How do protein hormones act on target cells?
Back: Bind to cell surface receptors
Front: What happens if receptor mutations occur?
Back: Diseases arise (e.g., inactivation or nonhormonal pathway activation)
Front: What are steroid hormones derived from?
Back: Cholesterol
Front: Where are steroid hormones produced?
Back: Adrenal cortex, ovaries, testes
Front: Are steroid hormones stored in large amounts?
Back: No, they are synthesized rapidly as needed
Front: Are steroid hormones hydrophobic or hydrophilic?
Back: Hydrophobic; they easily pass through cell membranes
Front: How are steroid hormones transported in blood?
Back: By carrier proteins
Front: How do steroid hormones act compared to protein hormones?
Back: Slower onset but longer-lasting effects
Front: What are modified amino acid hormones derived from?
Back: Tyrosine
Front: Give examples of modified amino acid hormones.
Back: Thyroid hormones, epinephrine, norepinephrine
Front: How are modified amino acid hormones transported?
Back: Via carrier proteins (mostly water-insoluble)
Front: Where do modified amino acid hormones act?
Back: Intracellular receptors
Front: What is the half-life of modified amino acid hormones?
Back: Short (<5 min)
Front: What causes Cushing’s Syndrome in horses?
Back: Pituitary Pars Intermedia Dysfunction (PPID) – adenoma of the pars intermedia
Front: How does Cushing’s affect the hypothalamus?
Back: Alters body temperature, appetite, shedding
Front: What is the pathognomonic sign of Cushing’s in horses?
Back: Long, curly hair coat
Front: What are other clinical signs of Cushing’s?
Back: PU/PD, muscle weakness, abnormal fat distribution, increased infections
Front: How is Cushing’s diagnosed?
Back: ACTH concentrations, blood cortisol response, thyrotropin-releasing hormone (TRH) test
Front: What is the treatment for Cushing’s?
Back: Pergolide (dopaminergic receptor agonist), body hair clipping, supportive care
Front: Is hyperthyroidism in horses commonly misdiagnosed?
Back: Yes
Front: What are the two types of hyperthyroidism?
Back:
Primary: Thyroid gland dysfunction
Secondary: Anterior pituitary dysfunction → low TSH
Front: What are clinical signs of hyperthyroidism in foals?
Back: Weakness, poor suckling, fine hair coat, tendon laxity, low body temperature
Front: What are clinical signs of hyperthyroidism in adult horses?
Back: Lethargy, low heart rate, obesity, laminitis, exercise intolerance
Front: How is hyperthyroidism diagnosed?
Back: Thyroid hormone levels (unreliable), TRH response test, response to hormone supplementation
Front: What is the treatment for hyperthyroidism?
Back: Thyroid hormone supplementation (weaning required)
Front: What causes hypothyroidism in sheep/goats?
Back: Iodine deficiency, thyrotoxic plants
Front: What happens when T3/T4 levels are low?
Back: Increased TSH → thyroid gland enlargement
Front: What are the clinical signs of hypothyroidism in sheep/goats?
Back: Poor wool quality, dry skin, tendon laxity, poor reproductive performance
Front: How is hypothyroidism diagnosed?
Back: Clinical signs + low iodine levels
Front: What is the treatment for hypothyroidism?
Back: Iodine supplementation
Front: What causes hyperparathyroidism?
Back: Nutritional imbalance (Ca:P ratio), oxalate-rich plants, iatrogenic causes
Front: What hormone is involved in hyperparathyroidism?
Back: Parathyroid hormone (PTH) → bone calcium resorption
Front: What are clinical signs of hyperparathyroidism?
Back: Lameness, loose teeth, spontaneous fractures, inability to rise
Front: How is hyperparathyroidism diagnosed?
Back: Radiographs, dietary analysis
Front: How is hyperparathyroidism treated?
Back: Correct mineral imbalance, prevent with proper diet