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Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Endocrinology is the study of

A

hormones, their receptors, the intracellular signalling pathways and their associated diseases.

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2
Q

Endocrine glands are…

A

ductless and release hormones directly into the blood.

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3
Q

Endocrine glands allow

A

rapid adaptive changes, integration of whole body physiology, chronic maintenance of metabolic environment

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4
Q

Examples of endocrine glands

A

Thyroid, adrenal and beta cells of the pancreas

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5
Q

Exocrine glands secrete

A

through a duct to site of action

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6
Q

Examples of exocrine glands

A

submandibular, parotid, pancreas- amylase and lipase

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7
Q

3 types of hormone action

A

endocrine - blood-borne acting at distant sites
paracrine - acting on adjacent cells
autocrine - acts on itself

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8
Q

2 types of hormones

A

Water soluble

Fat soluble

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9
Q

Water soluble hormones

A

Transported unbound
Bind to surface receptor on cells
Short half-life
Cleared fast

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10
Q

Examples of water soluble hormones

A

Peptides and monoamines (both stored in vesicles before secretion)

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11
Q

Fat soluble hormones

A

Transported bound to protein
Diffuse into cells
Long half-life
Cleared slowly

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12
Q

Examples of fat soluble hormones

A

Thyroid hormone and steroids (synthesised on demand)

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13
Q

Hormone classes

A

Peptides e.g insulin
Amines e.g. dopamine, adrenaline and noradrenaline
Iodothyronines
Cholesterol derivatives and steroids

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14
Q

Hormone classes - peptides

A 
E.g Insulin
Stored in secretory granules
Hydrophilic and water soluble
Released in pulses or bursts
Clearing by tissue
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15
Q

Synthesis of peptide hormone

A

Synthesis:
Preprohormone –> prohormone

Packaging:
Prohormone –> hormone

Storage and secretion:
hormone

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16
Q

Insulin activation

A
  1. Binds to insulin receptors
  2. Results in phosphorylation of the receptor and the activation of secondary messenger - Tyrosine kinase
  3. Phosphorylation of signal molecules
  4. Cascade effect
  5. Glucose uptake
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17
Q

Amine synthesis from Phenylalanine

A

Phenylalanine –> L-Tyrosine –> L-Dopa –> Dopamine –> noradrenaline –> adrenaline

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18
Q

Noradrenaline and adrenaline are broken down by

A

COMT (Catechol-O-methyl transferase)

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19
Q

Noradrenaline and adrenaline are broken down into

A

Normetanephrine and metanephrine.

Serum levels of these acts as indicators for the activity of noradrenaline and adrenaline.

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20
Q

NAd and Ad binding to alpha receptors causes

A

VasoConstriction
Bowel muscle contraction
Sweating
Anxiety

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21
Q

NAd and Ad binding to beta receptors causes

A

VasoDilation
Increase heart rate
Increases force of contractility
Relaxation of bronchial smooth muscles

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22
Q

Iodothyronines are not

A

water soluble so are bound to protein (Thyroid-binding globulin TBG)

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23
Q

T3

A

More active

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24
Q

T4

A

Less active but more is produced

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25
Q

Cholesterol derivative - Vitamin D

A

Fat soluble
Enters cell directly to bind to nucleus and stimulate mRNA production
Transported by vitamin D binding protein

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26
Q

Adrenocortical and gonadal steroid examples

A

cortisol, aldosterone, testosterone, oestrogen, progesterone.
95% protein bond

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27
Q

Hormone receptor locations and examples

A

Cell membrane - peptide e.g. insulin

Cytoplasm - steroids:

  • Cortisol
  • aldosterone
  • Androgens e.g. testosterone
  • Progesterone

Nucleus - thyroid hormones:

  • Thyroid hormones
  • Oestrogen
  • Vitamin
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28
Q

Hormone secretion patterns

A

Continuous release e.g prolactin
Pulsatile e.g. insulin
Circadian rhythm e.g. ACTH, prolactin, GH, TSH, cortisol

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29
Q

GH is inhibited by

A

Somatostatin and GHRH (negative feedback)

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30
Q

5 ways to control hormone action

A
  1. Hormone metabolism
  2. Hormone receptor induction
  3. Hormone receptor down regulation - hormone secreted in large quantities
  4. Synergism - 2 hormones amplify effect e.g. glucagon with adrenaline both increase sugar levels
  5. Antagonism - glucagon antagonises insulin
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31
Q

Cavernous sinus structures

A 
Abducens nerve (VI) and carotid artery. 
Can be affected in pituitary pathology.
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32
Q

Anterior pituitary is sometimes referred to as

A

adenophysis

33
Q

Posterior pituitary is sometimes referred to as

A

neurohypophysis

34
Q

Hypophysiotrophic hormones (6) released by the hypothalamus

A
  1. Corticotropin-releasing hormone (CRH)
  2. GHRH
  3. Somatostatin
  4. Thyrotropin-releasing hormone (TRH)
  5. GnRH
  6. Dopamine
35
Q

Blood supply of anterior pituitary gland

A

No arterial blood supply.

Receives blood through portal venous circulation.

36
Q

Hormones of the anterior pituitary

A

6 Peptide hormones:

  1. FSH
  2. LH
  3. Adrenocorticotrophic hormone (ACTH)
  4. TSH
  5. Prolactin
  6. GH
37
Q

Functions of FSH and LH

A

Target the gonads
Stimulate germ cell development
FSH stimulates oestrogen release
Positive feedback is the release of oestrogen and stimulates LH.
LH stimulates the release of the egg which in turn stimulates progesterone release –> thickening of the uterine wall.
In men, LH stimulates Leydig cells –> testosterone release

38
Q

Functions of GH

A

Stimulates growth and protein synthesis
Effect on whole body
Stimulates glucogenesis and inhibits insulin
Works on adipose tissue to breakdown fat
Acts on Liver to increase protein synthesis and stimulate IGF-1 –> acts on skeleton to increase cartilage proliferation

39
Q

What is measured to reflect GH levels

A

IGF-1

40
Q

Functions of ACTH

A

Stimulates adrenal cortex to secrete Cortisol from zona fasiculata
Androgen release from zona reticularis
Ad release from adrenal medulla
Cortisol - breakdown proteins, fats, carbs, anti-inflammatory effects, overcome stress.

41
Q

TSH functions

A

Stimulates thyroid hormone release:

  • controls rate of metabolic reactions
  • accelerate food metabolism
  • increases protein synthesis
  • stimulation of carbohydrate metabolism
  • enhances fat metabolism
  • increase ventilation rate
  • increase CO and HR
42
Q

T3 half life

A

1 day

43
Q

T4 half life

A

5-7 days

44
Q

Prolactin functions

A

Stimulates breasts to produce milk and breast development.

Inhibited by dopamine

45
Q

Posterior pituitary hormones are produced in

A

the hypothalamus. Stored in the posterior pituitary

46
Q

Posterior pituitary originates

A

neuronal tissue with large quantities of glial type cells

47
Q

Vasopressin/ADH is synthesised in

A

supraoptic nucleus

48
Q

Oxytocin is synthesised in

A

paraventricular nucleus

49
Q

Vasopressin/ADH functions

A
  • Decrease H20 secretion in urine
  • Vasoconstriction –> increase BP
  • Stimulates ACTH release to increase aldosterone release to further increase fluid retention
50
Q

Vasopressin is released in response to

A
  • decreased blood volume
  • trauma
  • stress
  • increase blood CO2
  • decreased blood O2
  • increased osmotic pressure of blood
51
Q

Oxytocin functions

A

-Ejection of milk during breast feeding
Pregnancy:
-contraction of uterine smooth muscles until baby is born
-promotes onset of labour

52
Q

All pituitary and hypothalamic hormones act on

A

G-protein coupled receptors

53
Q

Diseases of the pituitary

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Sheehans - pituitary infarction after labour
  • Sarcoid/TB
54
Q

Vital presentations of pituitary tumour

A
  1. Pressure on local structures
    - Optic chiasm –> bitemporal hemianopia
    - Can cause hydrocephalus
    - Can get CSF leak
  2. Pressure on normal pituitary - hypopituitarism
  3. Functioning tumour - hyperpituitarism
    - Prolactinoma (treated using Cabergoline - dopamine agonist)
    - Acromegaly
    - Cushing’s Disease
55
Q

Diabetes mellitus definition

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both.
Hyperglycaemia results in serious microvascular (retinopathy, neuropathy, nephropathy) or macrovascular problems (strokes, renovascular disease) problems.

56
Q

Normal blood glucose levels

A

3.5 - 8 mmol/L

57
Q

Principal organ of glucose homeostasis

A

Liver

58
Q

How much glucose is produced and utilised each day

A

200g

59
Q

Where is glucose derived from?

A

90% from liver glycogen and hepatic gluconeogenesis.

Remainder from renal gluconeogenesis.

60
Q

Major consumer of glucose

A

Brain

Cannot utilise fatty acids are they cannot cross BBB.

61
Q

Glucose taken up by muscle is stored as

A

Glycogen or metabolised to lactate or CO2 and H2O

62
Q

Fat uses glucose for

A

Triglyceride synthesis

63
Q

Lipolysis of triglyceride releases

A

fatty acids + glycerol.

Glycerol used as a substrate for hepatic gluconeogenesis.

64
Q

Insulin functions

A
  • Suppress hepatic glucose output - decreases glycogenolysis and gluconeogenesis
  • Increases glucose uptake into muscle and fat tissue
65
Q

Biphasic insulin release

A
  • B-cells sense increase in glucose levels.
  • First phase response is rapid release of stored insulin.
  • If glucose levels remain high, second phase is initiated. This takes longer as more insulin must be synthesised.
66
Q

Glucagon functions

A
  • Increases hepatic glucose output - increases glycogenolysis and gluconeogenesis
  • Reduces peripheral uptake of glucose
  • Stimulates peripheral release of gluconeogenic precursors e.g. glycerol & AA
  • Stimulates lipolysis , muscle glycogenolysis and breakdown.
67
Q

Counter regulatory hormones which increase glucose production

A

Adrenaline, cortisol and GH

68
Q

Insulin produced by

A

beta cells of the Islets of Langerhans

69
Q

Precursor of insulin

A

proinsulin

70
Q

Proinsulin contains

A

Alpha and beta chain joined by C-peptide.

C-peptide is cleaved when insulin is formed

71
Q

Synthetic insulin does not have

A

C-peptide

72
Q

GLUT 1

A

Enables basal non-insulin stimulated glucose uptake

73
Q

GLUT 2

A

Found in Beta cells of pancreas, renal tubules and hepatocytes
Transport glucose into beta cells - enable them to sense glucose levels
only lets glucose in when there is a high concentration

74
Q

GLUT 3

A

Enables non-inulin stimulated glucose uptake into brain neurones and placenta.

75
Q

GLUT 4

A

Mediates peripheral action of insulin.

Channel through which glucose is taken up into muscle and adipose tissue after insulin binds to it.

76
Q

Insulin receptor activation

A
  1. Insulin binds
  2. Activates tyrosine kinase. Cascade response
  3. Migration of GLUT-4 transporter to the cell surface and increased transport of glucose into the cell
77
Q

Primary diabetes

A

Type 1 and Type 2

78
Q

Secondary diabetes due to

A
  • Pancreatic pathology e.g pancreatectomy, chronic pancreatitis, haemochromatosis
  • Endocrine induced disease e.g. Acromegaly or Cushing’s
  • Drug induced (thiazide)
  • Maturity onset diabetes of youth (MODY)
  • -> autosomal dominant form of type 2 diabetes altering beta cell function

Phase 2A (1 decks)

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