Endocrine system Flashcards

1
Q

What is the difference between endocrine, paracrine, and autocrine signalling?

A

Endocrine: travels via blood stream to distant targets
Paracrine: local hormones, nearby target cell
Autocrine: local hormone, targets itself

Neuroendocrine - neural cells that release chemical signals into the bloodstream

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2
Q

What are releasing hormones? Give an example

A

From hypothalamus to act on pituitary
GnRH

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3
Q

What are stimulating (or trophic) hormones? Give an example

A

From pituitary to act on another endocrine gland
TSH (thyroid stimulating hormone)

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4
Q

What are non-trophic hormones? Give an example

A

From an endocrine gland to target cells
eg Thyroid releases T3 and T4

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5
Q

What are amino hormones? Give an example

A

Derived from tyrosine
eg catecholamines adrenalin and noradrenalin from adrenal medulla
eg T3 and T4 from thyroid

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6
Q

What are peptide/protein hormones? Give an example

A

come from genes-> rough ER-> golgi -> vesicles
May undergo one or more post-translational
modifications including cleavage, glycosylation, disulfide bridging

eg Insulin, hGH

exocytosis is Ca dependent, vesicles are hydrophillic

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7
Q

What are steroid hormones? Give an example

A

Derived from cholesterol->pregnenolone
eg Glucocorticoids, Mineralocorticoids, Androgens, Estrogens and Progestins

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8
Q

What are some examples of second messengers?

A
  • cAMP or cGMP
    – phopholipids diacylglycerol and inositol
    triphosphate (DAG and IP3)
    – calcium
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9
Q

What are three changes that second messengers induce?

A
  • Alter phosphorylation (activity) of proteins
    – Alter permeability of membranes
    – Indirectly influence gene expression
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10
Q

Whats the difference between steroid/thyroid hormones and amino/peptide hormones?

A

Amino/peptide work through second messengers (extracellular receptors)
Steroid/thyroid work through intracellular receptors and act as transcription factors

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11
Q

Desricbe negative feedback loops?

A

Eg T3/T4 signal hypothalamus to stop TSH which stops thyroid from releasing T3/T4

most common

low T3/T4/ low metabolic rate stimulates hypothalamus to release TRH which stimulates ant pituitary to release TSH which stimulates thyroid follicular cells to release T3/T4 into blood stream
T3 levels increase which INHIBITS release of TRH and TSH

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12
Q

Describe positive feedback loops

A

Used to amplify a signal
E.g. Oxytocin (made in hypothalamus and released by posterior pituitary)

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13
Q

How are T3 and T4 synthesised, stored, and secreted?

A
  • Synthesised by follicular cells by iodination of thyrosine
  • Stored in follicular colloids on the surface of thyroglobin
  • Secreted by follicular cells (reuptake before release)
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14
Q

What are the actions of thyroid hormones?

A
  • Metabolic effects eg calorigenisis
  • Physiological effects eg RBC production, appetite
  • Reproductive effects eg fertility, onset of puberty
  • Developmental effects eg normal brain development
  • Cellular effects
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15
Q

What happens when thyroid function is impaired?

A

Hypothyroidism: bc disease of the thyroid (1st) or from lack of stimulation by TSH (2nd)
Hyperthyroidism: bc over activity of gland eg Graves disesase (autoimmune)

Hypothyroidism: coarse skin, weight gain
Hyperthyroidism: Clinical symptoms of grave disease: sweating, tremor, muscle weakness and loss of muscle mass, upper lid retraction, impaired eye movement, patchy depigmentation of the skin, clubbing of the fingers, goitre etc

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16
Q

What hormones does the posterior pituitary gland secrete?

A

Oxytocin and vasopressin (vasopressin = anti-diuretic
hormone (ADH))

17
Q

Where are osmoreceptors found?

A

Found in Hypothalamus

They send signals to the neuroendocrine cell in the hypothalamus that make vasopressin when plasma osmolality exceeds the threshold -> increase vasopressin secretion
SUPERRR sensitive

18
Q

Where are baroreceptors found and whats their function?

A

In the circulatory system
Activated by Decreased blood volume/pressure
Turn on vasopressin secretory cells
Not that sensitive

19
Q

What are the effects of ADH on the body?

A
  • Kidneys retain more water
  • Sweat glands stop
  • Arterioles constrict (inc BP)
20
Q

What stimulates ADH release?

A
  • Hi osmolality
  • Low blood volume
  • Low blood pressure
  • Angiotensin
  • Nicotine
  • Nausea
21
Q

What inhibits ADH release?

A
  • Low osmolality
  • Hi blood volume
  • Hi blood pressure
  • Atrial natriuretic peptide
  • EtOH
22
Q

What is Diabetes insipidus?

A

Inability to secrete or to respond to ADH

23
Q

Whats the difference between neurogenic and nephrogenic?

A

Neurogenic – hyposecretion of ADH due to damage of posterior pituitary
Nephrogenic – kidneys do not respond to ADH (pee a LOT, dehydration, thirst)

24
Q

What cells does oxytocin stimulate?

A
  • Smooth muscle cells in uterus: contract during birth
  • Myoepithelial cells in mamary glands: milk ejection
25
Q

What do alpha, beta, delta, and F-cells secrete?

Where in the pancreas?

A

Alpha: glucagon
Beta: insulin
Delta: somatostatin
F-cells: pancreatic polypeptides

islets of Langerhans

26
Q

What does glucagon do?

A

Inc blood glucose: Turns on glycogenolysis in liver, and gluconeogenesis

glycogenolysis (breakdown of glycogen into glucose in liver)
gluconeogenesis (converting other nutrients into glucose),

27
Q

What does insulin do?

A

Decrease blood glucose: glycogenesis

glycogenesis (accelerating transport of glucose into cells, converting glucose into glycogen)

28
Q

What does somatostatin do?

A

Decrease in secretion of insulin and glucagon and slows absorption of nutrients from gastrointestinal tract

29
Q

What do pancreatic polypeptides do?

A

Decrease in somatostatin secretion, gallbladder contraction and secretion of pancreatic enzymes

30
Q

What is Diabetes mellitus?

A
  • Cant produce/use insulin
  • Elevation of blood glucose (hyperglycemia) and loss of glucose in the urine (glucosuria)
31
Q

Define polyuria

A

Excessive urine production due to inability of kidneys to reabsorb water

32
Q

Define polydipsia

A

Excessive thirst

33
Q

Define polyphagia

A

Excessive eating

34
Q

What is the difference between type I and type II diabetes?

A

Type I:
- Autoimmune disorder (Ab against beta cells)
- Cells use fatty acids to produce ATP (glucose cant enter cells)
- By-product are ketones – ketoacidosis
- Weight loos, arteriosclerosis, cardiovascular problems, cataracts, kidney failure, death
Type II:
- non-insulin dependent
- High glucose levels in blood regulated by controlled diet, exercise and weight loss

35
Q

What cells in the pineal gland secrete what hormone?

A

Pinealocytes
Release melatonin

36
Q

What happens when pineal gland function is impaired?

A

SAD (too much melatonin)
Jet lag

37
Q

What happens when theres hormonal dysfunction?

A
  • Autoimmune diseases: develop antibodies for some of their own receptors (hypothyroidism causing cretinism) or antibody causes hyperfunction (hyperthyroidism caused by Grave’s disease)
  • Gene mutations for receptors or G proteins (hypocalcemia, acromegaly, diabetes mellitus)