Endocrine And Reproduction Flashcards

1
Q

How is insulin secretion regulated?

A

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.

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2
Q

Metabolic actions of insulin?

A
Glucose oxidation
Glycogenesis
Lipogenesis
Protein synthesis
Anabolic hormone- fed state
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3
Q

How is glucagon release regulated?

A

Glucagon is produced by alpha endocrine pancreatic cells in response to low plasma glucose. Promotes gluconeogenesis and glycogenolysis

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4
Q

Insulin and the liver?

A

Liver does not require insulin for glucose uptake, just increases rate

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5
Q

Cellular action of insulin

A

Insulin increases glucose uptake into cells by adding more GLUT4 transporters onto the cell membrane

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6
Q

Insulin and the CNS

A

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.

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7
Q

Common clinical signs and serum biochemistry of diabetes mellitus?

A

Clinical signs? Weight loss due to decrease protein synthesis,
Polydipsia and polyuria, CNS signs, coma

Serum biochemistry? Hyperglycaemia, hyperlipidaemia, glycouria

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8
Q

Explain the pathophysiology of diabetic ketoacidosis

A

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.

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9
Q

Explain how thyroid secretion is controlled?

A

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

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10
Q

How are thyroid hormones transported?

A

Transported in blood bound to TBG, serves as a depot for several days.

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11
Q

Main actions of thyroid hormones?

A
Normal growth and development
Increases BMR
Cardiovascular stimulant
Glucose and fat utilisation for energy 
Dominant role in controlling metabolism
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12
Q

Common clinical signs for hypothyroidism

A
Too little TH
weigh gain
Cold intolerance
Poor exercise tolerance
Mental dullness
High blood cholesterol
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13
Q

Common clinical signs of hyperthyroidism

A
Too high TH
weight loss
Hyperthermia
High heart rate
Excitable
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14
Q

Testing for hypothyroidism

A

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

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15
Q

Testing for hyperthyroidism

A

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

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16
Q

HPO axis with regards to adrenal gland

A

Hypothalamus –> ACTHRH- AntPit–> ACTH- adrenal gland

17
Q

Secretion, regulation and actions of cortisol

A

Secreted from zona fasciculata in adrenal cortex in response to stress.
Causes gluconeogenesis, lipolysis, immune suppressant, anti inflammatory

18
Q

Secretion, regulation and actions of aldosterone

A

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.

19
Q

Blood tests for hypo and hyperadrenocorticism

A

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

20
Q

Two types of hypoadrenocortisism

A

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

21
Q

Two types of hyperadrenocorticism

A

Pituitary dependent
Constant signal form brain
High cortisol, high ACTH

Adrenal dependent
Trying normal homeostasis, adrenal gland just keep producing
High cortisol, low ACTH

22
Q

Clinical signs of hyperadrenocorticism

A

Hyperglycaemia
Polyuria and polydipsia
Tissue wasting- pot belly
Muscle weakness

23
Q

Clinical signs of aldosterone deficiency

A

Hyperkalaemia

Low sodium

24
Q

Describe calcium homeostasis

A

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.

25
Q

Describe phosphate homeostasis

A

Linked with calcium homeostasis
Vit D3, same as calcium
PTH increases renal excretion

26
Q

Explain renal secondary hyperparathyroidism

A

With chronic renal failure, cannot convert enough VitD to active form VitD3
Kidneys do not adequately excite phosphate.
PTH is used to decrease phosphate levels
No VitD3 to control PTH levels
High levels of PTH —hyoerparathyroidism

27
Q

Blood tests for calcium metabolism

A

Total serum ca2+

PTH levels
Primary hypercalcaemia, low PTH
Cancer causing hypercalcaemia high PTH

28
Q

Blood tests for GH disorders

A

Basal GH concentration- difficult

Basal IGF-1 better

29
Q

Secretion and actions of growth hormone

A

Hypothalamus - GHRH
AntPit- GH
Liver- IGF-1 —> stimulates effects

Effects? Bone and cartilage growth, protein synthesis, lipolysis

30
Q

Outline lactogenesis

A

Acquisition of secretory cells
Beginning on milk production
Synchronised with parturition
Influenced by cortisol, Prolactin, Oestrogen

31
Q

Outline galatopoiesis

A

Maintaining milk secretion, requires rm oval of milk
Prolactin maintains alveolar cell metabolism
GH upholds secretion

32
Q

Testosterone
Secreted from?
Actions?
In females??

A

Secreted by testis by interstitial cells of leydig
Actions- promotes spermatogenesis, anabolic growth, aggressive behaviour

Females? Substrate for oestradiol synthesis, high levels inhibit GnRH, LH, FSH, suppress oestrous cycle, abnormal masculinisation

33
Q

Oestrogen
Secreted?
Actions?

A

Secreted by follicles in ovaries
Keeps oestrous cycle
Female puberty and sexual behaviour

34
Q

Progesterone
Secreted?
Action?

A

Secreted by CL and placenta

Maintains pregnancy, inhibits reproductive activity

35
Q

Outline functions of GnRH

A

Drives production of anterior pituitary hormones- gonadotropins LH and FSH

36
Q

Outline functions of LH and FSH

A

FSH
Females- growth and recruitment of follicles, oestrogen synthesis
Makes- spermatogenesis

LH
Females- precursor for oestrogen production, ovulation, maintains CL
Males- testosterone synthesis by leydig cells

37
Q

Describes how the foetus initiates parturition

A

Foetal stress- cortisol causes progesterone to be converted to oestrogen which makes the repro tract secrete lubrication and initiates myometrial contractions. Cortisol also cause PGF to induce luteolyisis and produce relaxin which causes pelvic ligament stretching