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Block 1 > Introduction To Endocrinology > Flashcards

Introduction To Endocrinology Flashcards

1
Q

Define endocrinology.

A

The study of endocrine glands (tissues) + the substances they secrete

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2
Q

Define endocrine gland.

A

A gland that makes + secretes hormones into the bloodstream through which they travel to affect distant targets

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3
Q

Define hormone.

A

A chemical substance produced by cells + released especially into the blood + having a specific effect on cells or organs usually at a distance from the place of origin

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4
Q

Define exocrine gland.

A

A gland that secretes its products through ducts opening onto an epithelium rather than directly into the blood

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5
Q

What is endocrine secretion?

A

Secretion of a hormone into the blood stream to act on a distal tissue

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6
Q

What is the definition of endocrine?

A

Of, relating to, promoted by, or being a substance (hormone) secreted be cells of a gland into the bloodstream through which is travels to act on distant targets

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7
Q

What is the definition of paracrine?

A

Of, relating to, promoted by, or being a substance secreted by a cell + acting on adjacent cells

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8
Q

What is the definition of autocrine?

A

Of, relating to, promoted by, or being a substance secreted by a cell + acting on surface receptors of the same cell

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9
Q

What type of chemical messengers exist?

A

Neurotransmitters
Neuroendocrine hormones
Endocrine hormones
Cytokines (peptides with autocrine, paracrine + endocrine functions)

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10
Q

Give a brief overview of the endocrine system.

A
  1. The endocrine system receives chemical + physical stimuli
  2. It responds by releasing a chemical signal e.g. hormone
  3. The signal will elicit a change in the tissue e.g. change in metabolic rate or increased secretion
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11
Q

What are the main endocrine organs?

A 
Hypothalamus
Pituitary 
Thyroid
Thymus
Adrenal
Pancreas 
Kidney 
Ovary 
Uterus
Testes
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12
Q

What tissues have an endocrine function?

A 
Heart
Gut
Liver 
Adipocytes
Placenta
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13
Q

What are the main molecular types of hormones?

A

Polypeptides
Modified AAs
Steroids

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14
Q

Gives some examples of hormones derived from amino acids.

A
  • Single AAs e.g. catecholamines + 5-HT
  • Dipeptides e.g. thyroid hormones
  • Small peptides e.g. TRH, vasopressin + somatostatin
  • Intermediate size e.g. insulin, PTH
  • Complex polypeptides e.g. gonadotrophs (FSH, TSH + LH)
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15
Q

Gives some examples of hormones derived from lipid precursors.

A
  • Cholesterol e.g. steroids (Cortisol, sex steroids + vitamin D)
  • FAs e.g. prostaglandins
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16
Q

What are the characteristics of peptide and catecholamine hormones?

A

Rapid changes in [plasma]

Short (sec-min) T/12

Cell membrane receptor

Activate preformed enzymes, secretory granules, constitutive + burst

Rapid (sec-min) affect

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17
Q

What are the characteristics of steroid and thyroid hormones?

A

Slow fluctuations in [plasma]

Long (min-days) T1/2

IC receptor

Stimulate protein synthesis, direct rapid passage, related to secretion rate

Slow (hrs-days) affect

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18
Q

How are protein and peptide hormones synthesized and secreted?

A
  1. Gene transcription in nucleus
  2. mRNA goes to RER
  3. Translated on RER
  4. Post-translational processing in golgi
  5. Packaging into secretory vesicles
  6. Exocytosis
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19
Q

How are steroid hormones synthesized and secreted?

A
  1. Hydrolysis of esters + release of cholesterol (or cholesterol uptake)
  2. Cholesterol converted to pregnenolone in mitochondrion
  3. Processing in SER
  4. Diffusion out of cell
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20
Q

What occurs in post-translational processing of Parathyroid Hormone (PTH)?

A
  1. Initially synthesized as long polypeptide pre-Pro-PTH (115 residues)
  2. Enters ER + cleaved to form pro-PTH (90 residues)
  3. Cleaved further in vesicle secretions
  4. PTH (84 residues) is secreted
21
Q

What is special about steroid hormone synthesis?

A

No gene activation; enzymatic processing

Not stored but processed when required

Type + activity of enzymes (tissue specific) determines type + amount of hormones (e.g. deiodinases + adrenal/gonads)

22
Q

What are the ways in which hormones can be transported in the blood?

A
  1. Water soluble hormones dissolve in blood

2. Hydrophobic/fat-soluble hormones (steroid + thyroid hormones) are transported bound to plasma binding proteins

23
Q

What is important when considering hormone transport by plasma protein binding?

A

Binding affinity

Bound hormone is considered to be inactive, protected from degradation + acts as a reservoir

24
Q

Where do water soluble hormones bind to exert their effect?

A

Cannot pass through membranes so bind to cell surface receptors e.g. GPCR, TKR

25
Q

What can happen when a hormone binds to a G-Protein Coupled Receptor (GPCR)?

A

Stimulatory or inhibitory effects on 1 of 2 pathways:

  • G proteins -> adenylate cyclase -> cAMP -> protein kinases
  • G proteins -> PLC -> IP3 -> Ca2+ released from ER
26
Q

What happens when a hormone binds to a Tyrosine Kinase Receptor (TKR)? What hormone binds to these?

A

Phosphorylation of receptor -> signalling cascades

E.G. insulin

27
Q

Where do hydrophobic hormones bind to exert their effect?

A

Bind to IC + cell surface receptors

28
Q

Explain steroid hormone receptor signalling briefly.

A

Protein carrier brings steroid hormone to cell surface receptor (rapid response)

OR

Steroid hormone is brought directly into the cell to bind a cytoplasmic receptor which moves into the nucleus activating transcription, translation + production of new proteins

29
Q

Explain the feedback axes of the most basic kind of endocrine gland.

A
  1. Gland receives chemical signal (trophic hormone) from another gland to increase or inhibit secretion
  2. Gland will secrete effector hormone
  3. Increased levels of effector hormone will cause:
    - Response in target cells
    - Inhibition of further trophic hormone secretion
30
Q

What is the difference between a tropic and trophic hormone?

A

Tropic hormones affect other endocrine glands whereas trophic hormones affect growth + development directly

31
Q

Describe the general endocrine feedback system of the HPA axis.

A

Hypothalamus -> releasing hormone -> anterior pituitary -> tropic hormone -> target endocrine gland -> hormone feedbacks to anterior pituitary + hypothalamus

32
Q

What are some examples of releasing and tropic hormones?

A 
CRH -> ACTH
LHRH -> LH, FSH
TRH -> TSH
PIH/GHRH -> PRL
GHRH/GHIH -> GH
33
Q

Briefly explain the concept of negative feedback.

A

Increased output from target cells or increased hormone will negatively feedback on trophic + tropic hormones inhibiting its further release

34
Q

Briefly explain the concept of positive feedback.

A

Increased levels of effector hormone cause increased levels of tropic + trophic hormone

35
Q

What is the main positive feedback example?

A

Oestrogen causing LH surge

36
Q

What is the difference between primary and secondary endocrine dysfunction?

A

Primary dysfunction is too much of effector hormone from endocrine organ whereas secondary dysfunction is overstimulation of the effector organ by excessive tropic hormone

37
Q

What can cause excessive hormone (hyper) production?

A

Neoplasm
Hyperplasia
Ectopic production

38
Q

What can cause too little hormone (hypo) production?

A 
Gland destruction (trauma, disease, autoimmune)
Not developed
39
Q

What can cause a failure to respond to a hormone (resistance)?

A

Receptor problems

IC signalling defects

40
Q

What effects does the glucocorticoid cortisol have?

A

Maintain muscle function + decrease muscle mass

Decrease bone function + increase bone resorption

Decreased connective tissue

Inhibit inflammatory + immune response

Maintain CO: decrease endothelial permeability + increased arteriolar tone

Facilitate maturation of foetus

Increased glomerular filtration + H2O clearance

Modulate emotional tone + wakefulness

41
Q

What is the disease caused by glucocorticoid excess? What are its symptoms?

A

Cushings syndrome

Symptoms:
Central weight gain but loss of musculature in extremities
Change in appearance (moon face)
Depression
Psychosis 
Insomnia 
Amenorrhoea
Poor libido
Thin skin
Bruising
Growth arrest
Back pain
Polyuria/polydipsia
42
Q

What is the treatment for excess glucocorticoid?

A

Reduce cortisol via surgery to remove tumour or drugs to inhibit cortisol production

43
Q

What is the disease caused by reduced glucocorticoids/mineralocorticoids? What are its symptoms?

A

Hypoadrenalism/Addison’s

Symptoms:
Weight loss
Anorexia
Weakness
Fever
Depression
Impotence/amenorrhoea
Nausea/vomiting
Diarrhoea/constipation
Confusion
Abdominal pain
Back pain
44
Q

What are the causes of reduced glucocorticoids/mineralocorticoids?

A

Destruction of adrenal cortex

Reduced glucocorticoid, mineralocorticoid + sex steroid production

45
Q

Describe the feedback loop of thyroid hormones.

A
  1. Hypothalamus secretes TRH
  2. TRH acts on anterior pituitary
  3. Anterior pituitary releases TSH
  4. TSH acts on thyroid gland to affect thyroid hormone synthesis + release
  5. Thyroid hormones can inhibit the hypothalamus + anterior pituitary
46
Q

What is meant by ‘free’ thyroid hormones?

A

T3/T4 are carried in the blood bound to albumin + TBG

Only a small amount of T3/T4 are unbound + free to have a biological effect on tissues - these are free hormones

47
Q

Describe the HPA axis feedback loop of cortisol.

A
  1. Hypothalamus produces CRH
  2. CRH acts on anterior pituitary
  3. Anterior pituitary produces ACTH
  4. ACTH acts on adrenal gland
  5. Cortisol is produced which can inhibit the anterior pituitary + hypothalamus
48
Q

What can cause an glucocorticoid excess?

A

Pituitary gland tumour

Ectopic ACTH syndrome (ACTH produced from a tumour in the lung, pancreas, thyroid or thymus gland)

Adrenal gland abnormality/tumour

Long-term use of corticosteroid medication

Familial

Block 1 (54 decks)

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