Endocrine And Reproduction Flashcards
(37 cards)
How is insulin secretion regulated?
Secreted from beta endocrine pancreatic cells within the islets of langerhans in response to high plasma glucose, high plasma amino acids. This is regulated by the autonomic nervous system, parasympathetic will increase insulin secretion. Sympathetic will inhibit secretion. GI hormones will also increase insulin release during a meal as an anticipatory release.
Metabolic actions of insulin?
Glucose oxidation Glycogenesis Lipogenesis Protein synthesis Anabolic hormone- fed state
How is glucagon release regulated?
Glucagon is produced by alpha endocrine pancreatic cells in response to low plasma glucose. Promotes gluconeogenesis and glycogenolysis
Insulin and the liver?
Liver does not require insulin for glucose uptake, just increases rate
Cellular action of insulin
Insulin increases glucose uptake into cells by adding more GLUT4 transporters onto the cell membrane
Insulin and the CNS
Neurones are not sensitive to insulin. Really susceptible to increase sin glucose and therefore need a tight control. Blood sugar concentration is directly proportional to glucose levels in CSF. Any changes in glucose concentration can lead to neuronal disturbances.
Common clinical signs and serum biochemistry of diabetes mellitus?
Clinical signs? Weight loss due to decrease protein synthesis,
Polydipsia and polyuria, CNS signs, coma
Serum biochemistry? Hyperglycaemia, hyperlipidaemia, glycouria
Explain the pathophysiology of diabetic ketoacidosis
Loss of glucose leads to protein and fat catabolism within cells. Liver breaks down fatty acids by beta oxidation to produce acetyl coA which can enter kerbs cycle. Any excess forms ketone bodies eg acetone. These ketone bodies are produced despite high blood glucose, the cells are starving.
Explain how thyroid secretion is controlled?
TRH is released by hypothalamus–> TSH released by Ant Pit. –> thyroid gland produces T3 and T4 within follicles.
This is controlled by negative feedback. When thyroid hormone levels are high, while cascade stops until they drop again
How are thyroid hormones transported?
Transported in blood bound to TBG, serves as a depot for several days.
Main actions of thyroid hormones?
Normal growth and development Increases BMR Cardiovascular stimulant Glucose and fat utilisation for energy Dominant role in controlling metabolism
Common clinical signs for hypothyroidism
Too little TH weigh gain Cold intolerance Poor exercise tolerance Mental dullness High blood cholesterol
Common clinical signs of hyperthyroidism
Too high TH weight loss Hyperthermia High heart rate Excitable
Testing for hypothyroidism
Serum total or free T4
Low baseline T4 with clinical signs, worth a trial of oral T4
TSH stimulation test
Take basal T4, inject TSH, repeat T4. In a normal animal, should increase. If not- oral T4
Testing for hyperthyroidism
Baseline T4 levels–high
T3 suppression test
Basal total T4, oral T3 for 3 days– normal animal should show T4 suppression
TRH stimulation test
Basal total T4, ink TRH, normal animal should increase T4
Little or no increase in hyperthyroidism cases, TRH is chronically suppressed and pathway responds poorly to TRH
HPO axis with regards to adrenal gland
Hypothalamus –> ACTHRH- AntPit–> ACTH- adrenal gland
Secretion, regulation and actions of cortisol
Secreted from zona fasciculata in adrenal cortex in response to stress.
Causes gluconeogenesis, lipolysis, immune suppressant, anti inflammatory
Secretion, regulation and actions of aldosterone
Secreted by zona glomerulosa in adrenal cortex in repossessed to high K+ and low BP (raas pathway) .
Causes increasd Na+ reabsorption and K+ secretion in distal convoluted tubule.
Blood tests for hypo and hyperadrenocorticism
ACTH stimulation test
Take basal cortisol blood level. Inject ACTH. take another blood sample. Normal animal cortisol should rise
Hypo- C will be low to begin with and stay low
Hyper- C will be high and stay high
Two types of hypoadrenocortisism
Primary- Addison’s disease
Destruction of adrenal cortex
Low cortisol, high ACTH
Acute hypovolaemic shock, bradycardia, low na and high k
Secondary - ACTH deficiency
Low cortisol, low ACTH
Will lead to atrophy of adrenal gland
Two types of hyperadrenocorticism
Pituitary dependent
Constant signal form brain
High cortisol, high ACTH
Adrenal dependent
Trying normal homeostasis, adrenal gland just keep producing
High cortisol, low ACTH
Clinical signs of hyperadrenocorticism
Hyperglycaemia
Polyuria and polydipsia
Tissue wasting- pot belly
Muscle weakness
Clinical signs of aldosterone deficiency
Hyperkalaemia
Low sodium
Describe calcium homeostasis
Parathyroid hormone (parathyroid gland)
Controlled by free calcium in blood, released in response to low ca. Increase absorption from GI tract and release ca from bone
Negative feedback
Vitamin D3 activated by parathyroid hormone, (diet and sun)
Enhances ca uptake from small intestine. Negative feedback
Calcitonin (parafollicular cells in thyroid gland)
Released with high ca. Increase urinary loss and decreases gut absorption.
