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
What do alpha, beta, delta, and F-cells secrete? | Where in the pancreas?
Alpha: glucagon Beta: insulin Delta: somatostatin F-cells: pancreatic polypeptides | islets of Langerhans
26
What does glucagon do?
Inc blood glucose: Turns on glycogenolysis in liver, and gluconeogenesis ## Footnote glycogenolysis (breakdown of glycogen into glucose in liver) gluconeogenesis (converting other nutrients into glucose),
27
What does insulin do?
Decrease blood glucose: glycogenesis ## Footnote glycogenesis (accelerating transport of glucose into cells, converting glucose into glycogen)
28
What does somatostatin do?
Decrease in secretion of insulin and glucagon and slows absorption of nutrients from gastrointestinal tract
29
What do pancreatic polypeptides do?
Decrease in somatostatin secretion, gallbladder contraction and secretion of pancreatic enzymes
30
What is Diabetes mellitus?
- Cant produce/use insulin - Elevation of blood glucose (hyperglycemia) and loss of glucose in the urine (glucosuria)
31
Define polyuria
Excessive urine production due to inability of kidneys to reabsorb water
32
Define polydipsia
Excessive thirst
33
Define polyphagia
Excessive eating
34
What is the difference between type I and type II diabetes?
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
What cells in the pineal gland secrete what hormone?
Pinealocytes Release melatonin
36
What happens when pineal gland function is impaired?
SAD (too much melatonin) Jet lag
37
What happens when theres hormonal dysfunction?
- 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)