Endocrinology Basics (y1/2) Flashcards

1
Q

Where do lipid soluble hormones bind?

A

receptors in cytoplasm or nucleus

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2
Q

Where do water soluble hormones bind?

A

Receptors on cell surface

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3
Q

Where are the exocrine cells of the pancreas located?

A

Acini (clusters)

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4
Q

Where are the endocrine cells of the panrcreas located?

A

Amongst the acini - islets of langerhans

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5
Q

What are the 4 cell types of the pancreatic islet and what do they each secrete?

A

Alpha - glucagon
Beta - insulin
Delta - somatostatin
F cell - pancreatic polypeptide

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6
Q

What are the 3 targets of insulin?

A

Liver
Muscle
Adipose Tissue

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7
Q

Which 3 organs are NOT insulin dependent?

A

Brain (although NEEDS glucose)
Kidney
Intestine

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8
Q

What action does glucose have at a molecular level?

A

Inserts GLUT 4 transporters into cell wall.

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9
Q

What action does glucose have at a cellular level?

A

inc glucose metabolism

inc glycogen, protein and triglyceride synthesis

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10
Q

What action does glucose have at a tissue level?

A

decrease plasma glucose by:
inc transport into cells
OR
inc metabolic use

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11
Q

Apart from inc blood glucose, what 3 things may increase insulin secretion?

A

Inc plasma AA’s
Anticipatory release of GI hormones
Inc Parasympathetic activity during/post meal

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12
Q

What is the role of glucagon at a tissue level?

A

Glycogenolysis and Gluconeogenesis

Ketogenesis

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13
Q

Which tissue is the target of glucagon?

A

Liver

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14
Q

What is glucagon released in response to?

A

Dec plasma glucose
Inc plasma AA’s
Parasympathetic & SYMP (stress) activity

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15
Q

What is the role of somatostatin?

A

Decrease Growth Hormone

Stop insulin/glucagon release

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16
Q

What is the role of Pancreatic Polypeptide?

A

Unknown! increases after meals

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17
Q

What is Type 1 DM?

A

Inadequate insulin secretion

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18
Q

What is Type 2 DM?

A

Abnormal target cell response to insulin

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19
Q

What are the signs of DM?

A

Hyperglycaemia
Weight loss - low protein synth and low glucose cause muscle breakdown
PU/PD
ketoacidosis

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20
Q

What does the pituitary consist of?

A

2 fused glands:
AP: endocrine
PP: neural extension

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21
Q

What is secreted by the Posterior Pituitary?

A

Oxytocin

ADH

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22
Q

Where are ADH and oxytocin produced?

A

Hypothalamus

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23
Q

How do the hypothalamic hormones reach the AP?

A

Portal Capillary System

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24
Q

How do the hypothalamic hormones reach the PP?

A

In vesicles down neuron cell body

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25
Q

What are the 6 hormones secreted by the AP?

A

FLAT PiG:

FSH
LH
ACTH
TSH
Prolactin
GH
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26
Q

What are the 3 releasing hormones that affect the AP?

A

TRH
CRH
GnRH

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27
Q

Where is thyroid hormone produced?

A

Thryoid Gland:

Follicular cells and T3/T4 assembled in colloid

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28
Q

How long does the supply of T3/T4 last in the thyroid?

A

2-3m

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29
Q

What is the main hormonal product of the thyroid gland?

A

T4

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30
Q

Which thyroid hormone is the most biologically active?

A

T3

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31
Q

Where is T3 produced?

A

Thyroid Gland

AND converted from T4 in peripheral tissues?

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32
Q

What is the role of the thyroid hormones?

A
Increase BMR
Enhanced CHO utilisation
Growth & development
CV stimulant 
Promotes milk production
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33
Q

On which two organs does negative feedback from the thyroid occur?

A

AP

Hypothalamus

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34
Q

What are the 4 major signs of hyperthyroidism?

A

inc appetite and WL
Hyperthermia
Inc HR
Excitable

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35
Q

What are the 5 major signs of hypothyroidism?

A
Weight gain but no inc appetite
Hypothermia
Lethargy/Poor exercise tolerance
Dec HR
Dullness
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36
Q

Where is the adrenal gland in relation to the kidney?

A

Craniomedially

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37
Q

What are the 4 layers of the adrenal gland and what do they produce?

A

Cortex:
Zona glomerulosa: mineralocorticoid
Zona fasiculata: glucocorticoid
Zona Reticularis: androgens

Medulla: Adrenaline/Noradrenaline

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38
Q

What is the role of cortisol?

A
Liver: gluconeogenesis
Other tissues: dec glucose uptake
Adipose: Lipolysis
Muscle: breakdown
Immune: suppression
39
Q

How do glucocorticoids aid vasoconstriction?

A

MUST be present for catecholamines to have vasoconstrictive effect

40
Q

Which hormone stimulates the production of cortisol and sex steroids?

A

ACTH

41
Q

What are the 3 causes of HAC?

A

Pituitary Dep HAC
Adrenal Dep HAC
Iatrogenic HAC

42
Q

What are the clinical signs of HAC?

A
hyperglycaemia
PUPD
Tissue wastage
Muscle weakness
Pot Belly
Hyperpigmentation
43
Q

what is the role of mineralocorticoids?

A

Sodium/potassium regulation in the blood eg Aldosterone

44
Q

What are the two major regulators of aldosterone?

A

Ang II and K+

45
Q

What two factors induce the release of catecholamines?

A

Stress

Hypoglycaemia

46
Q

What are the 4 major functions of catecholamines?

A

Increase Cardiac output means more blood to the skeletal muscle
Increase plasma glucose
Increase the breakdown of triglycerides

47
Q

What is the target of GH and what is the effect?

A

Liver - IGF-1 production

48
Q

What are the 3 effects of GH release?

A

Protein synthesis
Lipolysis
Inhibit glucose uptake

49
Q

What increases GH secretion? (4 S’s)

A

CNS input
Strenuous physical activity
Starvation/dec plasma glucose
Stress

50
Q

What is the pathway for the release of GH?

A

GHRH & somatostatin from hypothalamus –> GH from AP

51
Q

What is acromegaly caused by?

A

Chronic excess of GH

52
Q

What are the clincial fetaures of acromegaly and why?

A

Insulin resistant DM
Excessive extremity growth
Prognathism- bulging out of the lower jaw
Wide interdental space

53
Q

Where is melatonin secreted from?

A

Pineal gland

54
Q

What does melatonin control?

A

Circadian Rhythms

55
Q

When is melatonin secretion increased?

A

In the dark - causes drowsiness and lower temp

56
Q

Where is ANP secreted from and why?

A

Atrial cardiac myocytes when there is increased blood volume or atrial stretch.

57
Q

What is the role of ANP?

A

Counter RAAS - dec BV

58
Q

What is the role of leptin?

A

Inhibits appetite centre in hypothalamus

59
Q

GLUT 2 is always present on hepatocytes. True or False?

A

TRUE - glucose can always pass in or out of hepatocytes. Insulin aids this by adding GLUT4.

60
Q

Which insulin is good for acute ketoacidosis, but not regular use?

A

Crystalline Zinc

61
Q

What is the advantage of lente insulin?

A

very long DOA (8-24h) but 30m onset

62
Q

How does protamine zinc insulin have such a long DOA?

A

Protamine forms zinc crystals which slow insulin absorption

63
Q

How should an insulin overdose be treated?

A

Feed

Give IV glucose

64
Q

How does Metformin help in diabetes?

A

dec gluc abs from GIT
dec gluc output from liver
inc insulin receptor sensitivity

65
Q

How does Glipizide help in diabetes?

A

stimulates insulin secretion by preventing K+ exiting cell

66
Q

How can we treat an insulinoma medically?

A

Diazoxide - inhibits insulin secretion by activating K+ and inhibiting Ca in beta cell

67
Q

Why are ketone bodies produced in diabetes?

A

High glucose in plasma but cant enter cells where it is needed!!

68
Q

Where is TRH produced?

A

hypothalamus

69
Q

Where is TSH produced?

A

anterior pituitary

70
Q

Where is T3/T4 produced?

A

thyroid gland

71
Q

What is the most definitive test for hypothyroidism?

A
TSH stimulation:
- Basal T4
- Inject TSH
- Repeat T4
NORMAL: increase by >1.5x
72
Q

Name 2 thyroid hormone replacement therapies?

A

Levothyroxine (T4)

Liothyroxine (T3)

73
Q

Which animal has they greater T4 half life; Cats or Dogs? Why?

A

Dogs - increased levels of TBG. More hormone bound in plasma so cannot activate receptors.

74
Q

What test would you perform on a suspected hyperthyroid cat?

A

tT4 - if low end of ref interval, use fT4 too

75
Q

What is the T3 suppression test?

A

Basal tT4
Oral T3 for 3d
Normal: 50% suppression

76
Q

Name 3 treatments for hyperthyroidism in cats.

A

Methimazole
Carbimazole
Radioactive iodide

77
Q

Why treatment for feline hyperthyroidism requires hospitalisation for 1-4w?

A

Radioactive Iodide

78
Q

What are changes on a stress leucogram?

A

Segmented Neutrophilia
Monocytosis
Lymphocytopenia
Eosinopenia

79
Q

What are the 2 causes of HyperAC and what changes can you see on bloodwork for each?

A

Functioning Adrenal Tumour (inc cortisol, dec ACTH)

Functioning Pituitary Tumour (inc cortisol, inc ACTH)

80
Q

What are the signs of a primary hypoadrenocorticism?

A

Acute Hypovolaemic shock

Bradycardia (^K+)

81
Q

What are the 2 causes of HypoAC and what changes can you see on bloodwork for each?

A

Primary (dec cortisol, inc ACTH)

Secondary (dec cortisol, dec ACTH)

82
Q

What are the two tests for adrenocortical Dz?

A

ACTH Stim

Dex ST

83
Q

Name 2 SHORT acting glucocorticoids.

A

Hydrocortisone

Cortisone

84
Q

Name 3 intermediate acting glucocorticoids.

A

Prednisone
Prednisolone
Methylpred

85
Q

Name 2 LONG acting glucocorticoids.

A

Betamethasone

Dexmethasone

86
Q

Name 2 drugs commonly used to treat PDH orADH.

A

Trilostane - inhibits c/s synthesis

Mitotane - cytotoxic to ZF & ZR

87
Q

Which adrenal steroid inhibitor should NOT be used in pregnant animals, and why?

A

Trilostane - inhibits progesterone synthesis

88
Q

What is the main role of PTH?

A

Prevent hypocalcaemia - dec Ca in ECF stimulates secretion

89
Q

What is the main role of Calcitonin?

A

Prevent hypercalcaemia - inc Ca in ECF stimulates secretion

90
Q

What are the 3 main targets of PTH?

A

Bone
Intestine
Kidneys

91
Q

What is the main target of calcitonin?

A

Bone

92
Q

What are 3 ECG signs that IV Ca administration should be stopped?

A

Elevated ST segment
Short QT intervals
Arrhythmias

93
Q

State the 2 anti-diuretic drugs used to treat DI and state which is better and why.

A

Vasopressin

Desmopressin: better as less vasoconstriction and longer DOA