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Year 2 Semester 2 > Repro & Endocrine > Flashcards

Repro & Endocrine Flashcards

1
Q

The penile urethra sits within which muscle?

A

Corpus spongiosum

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2
Q

What is the name of the plexus taking away blood from the testes?

A

Pampiniform plexus

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3
Q

Where is each lobe of the pancreas located in the dog?

A

Right=within meso-duodenum

Left=within deep leaf of greater omentum

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4
Q

Which cells exist within islets of Langerhans in the pancreas?

A

Alpha and beta cells

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5
Q

How are exocrine cells arranged in the pancreas?

What about endocrine cells?

A

Exocrine=clusters called acini

Endocrine=islets of Langerhans

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6
Q

In the pancreas, what do acini produce?

A

Digestive enzymes that flow through ducts into the GI tract

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7
Q

Give 3 other catabolic hormones besides glucagon

A

Cortisol
Growth hormone
Catecholamines

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8
Q

What is the difference between type 1 and type 2 diabetes?

A

Type 1=inadequate insulin secretion

Type 2=abnormal target cell responsiveness

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9
Q

How does glucose enter cells?

Is this an active or passive process?

A

Through GLUT transporters

Passive (concentration gradient)

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10
Q

How does insulin increase glucose uptake in skeletal muscle, adipocytes and other cells?

A

Signals the cell to inset GLUT4 transporters into the membrane, allowing glucose to enter

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11
Q

What are the 3 things glucose can be converted to?

A

Glucose-6-phosphate
Glycogen
Fat

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12
Q

How is glucose taken up into hepatocytes?

A

Glucose enters the cell using GLUT2 transporters.
Insulin stimulates hexokinase to maintain a low intracellular concentration of glucose (converts glucose to glucose 6-phosphate)

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13
Q

What is the difference between presence of transporters in the membranes of hepatocytes compared with skeletal muscle, adipocytes and other cells?

A

Hepatocytes: GLUT2 transporters are ALWAYS present in the cell membrane (not insulin-dependant), transport in both directions.
Skeletal muscle cells: GLUT4 transporters are only present in the cell membrane when insulin signals the cell to insert them there. Only allow glucose to enter, not leave.

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14
Q

Are neurones sensitive to insulin?

A

No

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15
Q

How does excess glucose in the CSF affect neurones in the CNS?

A

Increases osmolarity of CSF, drawing water out of neurones

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16
Q

How does insulin decrease blood concentrations of glucose?

A

Increasing glycogen synthesis
Decreasing hepatic glycogenolysis
Decreasing gluconeogenesis
Increasing glucose transport into skeletal muscle cellls and adipocytes through GLUT4 transporters

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17
Q

What effect does insulin have on protein metabolism?

A

Increases protein synthesis and uptake of amino acids

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18
Q

What effect does insulin have on fat metabolism?

A

Increases fat synthesis and decreases lipolysis

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19
Q

What effect does insulin have on K+?

A

Increases uptake of K+ into skeletal muscle and fat cells by providing ATP to activate the NA+/K+ ATPase pump

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20
Q

Describe the structure of insulin and discuss species similarities

A

Insulin=2 peptides joined by a disulphide bridge.
Porcine and canine insulin molecules are identical, and only differ from human insulin by a single amino acid.
Feline and bovine insulin are similar in structure.
Water-soluble.

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21
Q

What kind of receptors does insulin bind to?

A

Tyrosine kinase membrane receptors

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22
Q

What is the plasma half-life of insulin?

What about biological half-life?

A

Plasma= 5-10 mins

Biological=several hours

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23
Q

In which species is the bulbourethral gland absent?

A

Dog

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24
Q

Sexual maturity is signalled by what?

A

Increased GnRH pulsatility

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25
Q

Where is insulin metabolised?

A

Liver and kidney

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26
Q

Which form of lente insulin has the longer duration?

A

Ultralente

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27
Q

What is the average duration of a soluble insulin formulation?
What about non-soluble?

A

Soluble=3-6 hours

Non-soluble=6-24 hours

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28
Q

What is meant by postprandial?

eg postprandial hyperglycaemia

A

After eating

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29
Q

Give 2 adverse effects of using exogenous insulin?

A 
Hypoglycaemia 
Insulin resistance (due to stress, insulin antibodies, or insulin receptor desensitisation)
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30
Q

How may stress induce exogenous insulin resistance?

A

By increasing secretion of adrenaline and corticosteroids

31
Q

What is an advantage of using an oral antihyperglycaemic over exogenous insulin?

A

Does not stimulate insulin secretion so does not cause hypoglycaemia

32
Q

Which channels does glipizide (anti-diabetic agent) block?

A

ATP-sensitive potassium channels

33
Q

Name a drug you could use to treat hyperinsulinism

How does it work?

A

Diazoxide
Activates potassium channels causing inhibition of voltage-gated Ca2+ channels
Inhibits insulin secretion

34
Q

What is the hormone relaxin produced by?

What does it do?

A

Produced by ovary and placenta in preparation for parturition
Softens the broad ligament, pelvic ligaments and sacroiliac joint

35
Q

Where is the thyroid located?

A

Two lobes located either side of the trachea just below the larynx

36
Q

Where is thyroid stimulating hormone released from?

A

Anterior pituitary gland

37
Q

Explain the thyroid hormone feedback loop

A

Thyroid stimulating hormone (TSH) is released by anterior pituitary in response to TRH secreted into the portal system from the hypothalamus. TSH causes the synthesis and secretion of T3 and T4 into the blood from follicular cells in thyroid. Elevated T3 inhibits release of TRH and TSH.
TSH also inhibits release of TRH from the hypothalamus

38
Q

What are the 5 functions of thyroid hormones?

A

Increase BMR
Normal growth and development (T3 causes increased GH secretion, maintenance of nerve function, hair growth)
Cardiovascular stimulant (increased CO)
Enhances CHO utilisation and lipolysis (increases LDL uptake by liver)
Promotes milk production

39
Q

Give some signs of hypothyroidism

A 
Poor exercise tolerance
Weight gain with no change in appetite
Intolerance to cold and hypothermia
Mental dullness
Increased blood cholesterol
Decreased heart rate
Bilateral symmetrical alopecia
40
Q

How much should T4 increase by after injecting TSH?

A

1.5 times

41
Q

T3 is how many times as active as T4?

A

3-5

42
Q

In thyroid hormone replacement therapy, what is used to replace:
T3
T4

A 
T3= Liothyronine
T4= Levothyroxine
43
Q

Explain the metabolism of thyroid hormones

A

30-40% T4 is converted to T3 in peripheral tissues
50% T4 is converted to reverse t3 (inactive)
20% T4 and 100% T3 form conjugates of glucoronide and sulphur in liver and are excreted in bile

44
Q

How are thyroid hormones transported and bound?

A

Transported bound to plasma proteins
Free protein binds to target receptors. Bound fraction provides a depot that lasts several days, as when free molecules bind to their target receptors, more molecules dissociate from bound protein.

45
Q

What are the 4 sigs of hyperthyroidism?

A

Weight loss with increased appetite
Hyperthermia
Increased heart rate
Excitable

46
Q

How can you test for hyperthyroidism?

A

Test for serum T4 levels (will be high)

47
Q

Describe the T3 suppression test when testing for hyperthyroidism

A

Take basal TT4 (total T4).
Give oral T3 for 3 days.
Resting T4 should be suppressed by >50%.
If little/no suppression -> producing excess T4 from thyroid gland.

48
Q

Which drugs can be used to treat hyperthyroidism?

A

Felimazole
Methimazole- inhibits synthesis of T3 and T4
Carbimazole (metabolised to methimazole)

49
Q

What is an alternative to surgical thyroidectomy?

What considerations are there?

A

Radioactive iodine
Destroys radioactive follicles
Treated animals need to be hospitalised for 1-4 weeks
Treated animals and excrete need to be handled carefully until radioactivity is gone

50
Q

What is a goitre?

What could cause it?

A

Enlarged thyroid gland

Could be due to tumour, or iodine deficiency

51
Q

Explain how an iodine deficiency could lead to an enlarged thyroid gland and hyperthyroidism

A

Lack of iodine in diet (eg lack in soil-sheep)/ substances that inhibit uptake
Can’t make thyroid hormones. Continually high TSH stimulates thyroid follicular cell growth. No negative feedback
Enlarged thyroid

52
Q

All steroid hormones from the adrenal cortex are formed from which molecule?
What is this then converted to?

A

Cholesterol

Pregnenalone

53
Q

How are steroid hormones transported?

A

Bound to plasma proteins

Lipid-soluble

54
Q

What is the mechanism of action of corticosteroids?

A

Act on intracellular receptors to alter mRNA synthesis

55
Q

What type of corticosteroid is aldosterone?

A

Mineralocorticoid

56
Q

What are the 3 normal functions of cortisol?

A

Increased blood glucose
Increased protein catabolism
Increased lipolysis

57
Q

What are the clinical signs of hyperadrenocorticism?

A 
Hyperglycaemia
PU and secondary PD
Tissue wasting
Muscle weakness
Pot belly
Increased skin pigment (synthesis of ACTH involves a precursor: POMC which stimulates MSH -> increases melanin production)
58
Q

What would you see on a stress leucogram?

A

Lymphocytopenia (decreased lymphocytes)
Monocytosis (increased monocytes)
Eosinopenia (decreased eosinophils)
Neutrophilia (increased neutrophils)

59
Q

What is a stress leucogram caused by?

A

Stress response or corticosteroid induced

60
Q

How you would distinguish a functioning adrenal tumour from pituitary-dependant hyperadrenocorticism?

A

Pituitary tumour- increased ACT

Adrenal tumour- decreased ACTH

61
Q

Name a common mineralocorticoid drug

A

Fludrocortisone

62
Q

What percentage of the body’s Ca2+ is found in bone?

What is it found as?

A

99%

Hydroxyapatite

63
Q

What is PTH secretion controlled by?

A

Serum-ionised calcium

64
Q

What are the effects of PTH?

A

Increases Ca2+ by affecting transport mechanisms in bone, kidney, and indirectly (via Vit D) the intestine
Increased absorption from GI tract
Increased osteoclastic activity so that Ca2+ is released from bone into blood
Increases renal excretion of phosphate

65
Q

What does vitamin D3 do?

A

Enhances Ca2+ uptake from small intestine

Increases intestinal absorption of phosphate and decreases renal excretion

66
Q

What does calcitonin do?

Where is it released from?

A

Decreases Ca2+, largely by affecting transport mechanisms in bone (less active bone remodelling by osteoclasts)
Comes from parafollicular cells of thyroid gland

67
Q

Why might you not administer calcium IV?

A

Can cause cardiac arrhythmias and arrest

68
Q

What is calcitriol?

A

Active vitamin D3

69
Q

Vasopressin and desmopressin are examples of what?

What are they used to diagnose/treat?

A

Anti-diuretics

Used to diagnose and treat diabetes insipidus

70
Q

What is somatotropin?

A

A growth hormone stimulant

71
Q

What does cabergoline do?

What is it used for?

A

Stops lactation
Induces oestrus and abortion in bitches
Treats false pregnancy

72
Q

What are the 6 hormones produced by the anterior pituitary gland?

A

FSH, LH, ACTH, TSH (thyroid stimulating hormone), GH and prolactin

73
Q

What are the 2 types of receptor for sex-steroid hormones?

A 
Nuclear receptors (slow)
Membrane receptors (fast)
74
Q

Name the commonly-used exogenous oestrogen

A

Oestradiol

Year 2 Semester 2 (16 decks)

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