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ASC111 > Module 2.3- Endocrine Disorders > Flashcards

Module 2.3- Endocrine Disorders Flashcards

1. Explain the regulation of the secretion of thyroid hormone and how thyroid hormone increases basal metabolic rate. 2. Define what is meant by primary, secondary and tertiary endocrine disorders. 3. Describe how hypersecretion of a particular hormone can influence metabolism. 4. Describe how hyposecretion of a particular hormone can influence metabolism.

1
Q

What is a tertiary (3 degree) endocrine disorder?

A

Problem originating in the hypothalamus

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2
Q

What is a secondary (2 degree) endocrine disorder?

A

Initial disorder is in the pituitary gland

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3
Q

What is a primary (1 degree) endocrine disorder?

A

The specific endocrine gland is dysfunctional

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4
Q

Outline the function of a normal endocrine system

A

Hypothalamus -> Pituitary gland -> Somatrophin increased -> Liver -> somatomedins produced, negative feedback from liver to pituitary gland -> peripheral tissues -> normal growth

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5
Q

Outline the endocrine pathway of someone suffering from hypopituitary dwarfism

A

Hypothalamus -> Pituitary gland (site of lesion)…

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6
Q

Outline the endocrine pathway of someone suffering from Gigantism (infantile) or Acromegaly (adult)

A

Hypothalamus-> Pituitary Gland (site of lesion) -> excess production of Somatotropin -> Liver -> excess production of Somatomedins -> Peripheral tissues -> Excessive growth

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7
Q

Outline the endocrine pathway of someone suffering from Laron dwarfism

A

Hypothalamus -> Pituitary Gland -> increased Somatotropin -> Liver (site of lesion/defect)…

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8
Q

Outline the endocrine pathway of someone suffering from End-organ Resistance dwarfism

A

Hypothalamus -> Pituitary Gland -> increased Somatotropin -> Liver, negative feedback to Pituitary Gland -> Peripheral tissues (site of lesion/defect)…

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9
Q

Outline the endocrine pathway of someone suffering from Acromegaly (adult) or gigantism (juvenile) where there is no lesion present.

A

Pancreas -> Somatocrinin -> Pituitary Gland -> Somatotrophin -> Liver -> Somatomedins -> peripheral tissues -> abnormal growth

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10
Q

What is pituitary dwarfism a deficiency of?

A

Adenohypophyseal (Hypopituitarism) and or Neurohypophyseal (Panhypopituitarism) hormones

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11
Q

What shouldn’t you confuse Pituitary Dwarfism (hypopituitarism and panhypopituitarism) with?

A

Achondrodysplasia

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12
Q

What is the difference between Gigantism and Acromegaly?

A

Both are excessive production of growth hormones but Gigantism is if it occurs before puberty and Acromegaly is if it occurs after growth plates close (adulthood).

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13
Q

Compare the levels of Serum Insulin-like Growth Factor-1 in some dog strains and how it affects growth

A 
Keeshound - 80 to 102 micrograms/l
Bassethound - 97 to 148 micrograms/l
Terrier - 184 micrograms/l
German shepherd - 257-303 micrograms/l
Great dane - 332 micrograms/l
New Foundland - 365-414 micrograms/l

Higher levels mean larger breed of dog

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14
Q

Describe changes to the physical appearance of the face of someone suffering from Acromegaly over their lifetime

A

Their face will appear normal and grow normally until after puberty. Post puberty, abnormal growth occurs and the jaw and forehead continue to grow. Eventually, the eyebrows, forehead, jaw, lips and eyes will protrude from the face and the nose will appear sunken.

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15
Q

Where is the site of a lesion/defect in someone suffering from Hypopituitary Dwarfism?

A

The Pituitary Gland

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16
Q

Where is the site of a lesion/defect in someone suffering from Gigantism/Acromegaly?

A

The Pituitary Gland

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17
Q

Where is the site of a lesion/defect in someone suffering from Laron Dwarfism?

A

The Liver

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18
Q

Where is the site of a lesion/defect in someone suffering from End-organ Resistance Dwarfism?

A

Peripheral tissues

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19
Q

What organ/gland can also be a cause of Acromegaly/Gigantism by producing Somatocrinin that interferes with the Pituitary Gland?

A

Pancreas

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20
Q

What is one example of an insulin endocrine disorder?

A

Diabetes Mellitus

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21
Q

What are all the types of Diabetes Mellitus?

A

Type I, Type II and Gestational Diabeties

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22
Q

What is type I Diabetes Mellitus?

A

Immune mediated destruction of pancreatic beta cells. No insulin is produced. Anyone with this is dependant on insulin injections to survive and will die within days or weeks without them.

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23
Q

What is type II Diabetes Mellitus?

A

“adult onset” diabetes. Either insulin resistance (caused by hormones or excessive stomach fat preventing the insulin from reaching muscle cells to deposit the glucose) AND/OR decreased insulin production. Individuals with this may or may not require insulin injections depending on the severity of insulin resistance. Will initiate as glucose intolerance

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24
Q

What is Gestational Diabetes Mellitus?

A

Insulin resistance caused by the hormones associated with pregnancy.

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25
Q

What is the glucose tolerance test?

A

A test used to determine if an individual has glucose resistance or Diabetes Mellitus based on the glucose levels found in the venous plasma after a 12 hour fast and then after they consume a set amount of glucose syrup.

26
Q

What are the glucose levels during the glucose tolerance test found in venous plasma of a normal person, glucose intolerant person and a person suffering from Diabetes Mellitus?

A

Normal:
Fasting- 7.8 mmol/L or >140 mg/dL

Diabetes Mellitus:
Fasting: >7.0 mmol/L or >126 mg/dL
2hr post- >11 mmol/L or >200 mg/dL

27
Q

What are four bad conditions or events that happen in an individual suffering from type I Diabetes Mellitus?

A

Tissue loss, metabolic acidosis (too much acid produced or not enough removed by/from body), hyperglycemia leading to polyuria (excessive urination), polyphagia (increased/excessive appetite)

28
Q

In dogs, when (age) does the peak prevalence of Diabetes Mellitus occur?

A

7-10 years old

29
Q

To diagnose Diabetes Mellitus in a dog, what two things must persistently occur?

A

Hyperglycaemia and glycosuria (excretion of glucose in the urea)

30
Q

Explain the interaction between the ‘Satiety centre’ and the ‘feeding centre’ of the hypothalamus in a dog

A

‘Satiety centre’ interacts with ‘feeding centre’ to control feed intake. Glucose levels affect ‘satiety centre’

31
Q

How does insulin deficiency (such as diabetes mellitus) effect the interaction between the ‘satiety centre’ and ‘feeding centre’ of the hypothalamus in a dog?

A

Insulin deficiency means the ‘feeding centre’ isn’t inhibited as glucose and insulin affect the ‘satiety centre’, which in turn affects the ‘feeding centre’. This leads to polyphagia (excessive hunger/increased appetite).

32
Q

What occurs as a result of failure to inhibit the ‘feeding centre’ of the hypothalamus in a dog?

A

Polyphagia (excessive hunger/increased appetite)

33
Q

What are the 4 classic signs of Diabetes Mellitus in dogs?

A

Polyuria (excessive urination)
Polydipsia (Excessive thirst)
Polyphagia (excessive hunger)
Weight loss

Although, Polyuria and polydipsia don’t develop until hyperglycaemia results in glycosuria (>10.1-12.3mmol/L blood [gluc])

34
Q

What are the treatments for diabetes mellitus in dogs?

A

Insulin therapy, diet changes and exercise

35
Q

What disorders can also occur concurrently with diabetus mellitus in dogs?

A

Pancreatitis, bacterial infections, recent oestrus, congestive heart failure, hyperadrenocorticism

36
Q

How is Diabetes Insipidus different to Diabetes Mellitus?

A

Insipidus is caused by deficiencies in secretion of ADH (vasopressin), Mellitus is caused by abnormalities in insulin secretion.

37
Q

What occurs in the body of an individual suffering from Diabetus Insipidus?

A

Deficiencies in secretion of ADH (vasopressin) from the posterior pituitary means renal water resorption, urine production and water balance can’t be properly regulated, impairing the individuals ability to conserve H2O and concentrate urine, causing Polyuria (Excessive urination) and Polydipsia (Excessive thirst)

38
Q

What are the typical symptoms of an individual suffering from Diabetes Insipidus?

A

Polyuria (Excessive urination) and Polydipsia (Excessive thirst)

39
Q

What are two syndromes/diseases caused by abnormal adrenocortical secretions?

A

Cushing’s syndrome and Addison’s disease

40
Q

What is Cushing’s syndrome?

A

Hyperadrencorticism, hypersecretion of adrenal cortex hormones.

41
Q

What are the known causes of Cushings syndrome?

A
  • Adenoma of adenohypohysis (excess ACTH, called cushings disease if the only cause)
  • Abnormal function of hypothalamus
  • Ectopic secretion ACTH by tumour elsewhere
  • Adenomas of adrenal cortex
  • Pharmacological administration of glucocorticoids
42
Q

What are the main effects of Cushing’s syndrome?

A
  • High blood glucose concentrations: Increased gluconeogenesis, decreased glucose utilisation
  • Decreased protein synthesis, muscle weakness, compromised immunity.
  • Increased salt retention, hypertension, oedema, skin/coat changes.
  • Polyuria (increased urination frequency) and Polydipsia (increased thirst)
43
Q

What are the available treatments for Cushing’s disease?

A

If a tumour is the cause, tumour removal.
Irradiation
Drugs that inhibit ACTH/CRH secretion

44
Q

What is Addison’s disease?

A

First degree hypoadrenalism

45
Q

What is the cause of Addison’s disease?

A

Atrophy of adrenal cortices due to autoimmune response, tumours and tuberculosis.

46
Q

What is the treatment for Addison’s disease?

A

Treatment with synthetic mineralocorticoids and glucocorticoids

47
Q

What are the main effects of Addison’s disease?

A 
Aldosterone deficiency, dehydration (excess Sodium excretion and Potassium retention).
Glucocorticoid deficiency (decreased blood glucose).
Melanin pigmentation (increased MSH production, skin blotches).
48
Q

List 4 disorders of the thyroid gland

A

Goitre, Hypothyroidism, Hyperthyroidism, Thyroid neoplasia.

49
Q

In regards to thyroid function, what does euthyroid mean?

A

“normal” Thyroid function

50
Q

In regards to thyroid function, what does hypothyroid mean?

A

Sub-normal thyroid function, deficiency in thyroid hormone

51
Q

In regards to thyroid function, what does hyperthyroid mean?

A

Excessive thyroid function

52
Q

What are the effects of hyperthyroidism?

A

Elevated T4-T3 levels, elevated basal metabolic rate, increased perspiration, rapid pulse (increased cardiac output, hypertension), increased body temperature (sensation of warmness), heat intolerance, warm moist palms, nervousness, anxiety, excitability, restlessness, insomnia, weight loss, muscle wasting, increased appetite, goitre (may or may not be present)

53
Q

What are the effects of hypothyroidism?

A

Decreased (or absent) T4-T3 levels, low basal metabolic rate (hypometabolism), decreased perspiration, slow pulse (decreased cardiac output, hypotension), lowered body temperature (sensation of coldness), cold intolerance, coarse dry skin, subdermal thickening, lethargy, decreased mentation, depression, paranoia, sleepiness, tiredness, weight gain, dry and brittle hair (with hair loss), oedema of face and eyelids, goitre (may or may not be present).

54
Q

When does cretinism occur in animals?

A

Developing animals and early post natal growth

55
Q

When does goitre occur with hypothyroidism?

A

When the removal of the negative feedback loop occurs, causing excess TSH secretion, resulting in cellular growth and proliferation in the thyroid (swelling, hyperplasia of follicular epithelium)

56
Q

What can cause Goitre to occur?

A

Iodine deficiency (primary cause)
Goitrogenic substances
Hereditary biosynthetic substances

57
Q

Can endemic (due to iron deficiency) goitre in ruminants cause congenital goitre?

A

Yes

58
Q

How do goitrogenic substances cause goitre?

A

They interfere with production of thyroid hormones.

59
Q

What is one example of a goitrogenic substance?

A

Brassica spp.

60
Q

When and how does genetic goitre occur in a species of animal?

A

Merion sheep, due to failure of thyroglobulin synthesis.

ASC111 (38 decks)

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