W3 - Endocrine System (Lecture) Flashcards

1
Q

What is the 2016 definition of a HM?

A

Long distance chemical mediator secreted by an endocrine gland into the blood which transports it to the target cell

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2
Q

What can be improved about the HM definition from 2016?

A

It’s not always blood and it’s not always ovr a ‘long’ distance

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3
Q

What are the 2 differences between NTMs and HMs?

A

NTM - released across synapse and therefore short distances, HM - released by gland and travel in circ system therefore longer distances

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4
Q

What are the 6 types of feedback loops?

A

Direct FL, first order FL, second order FL, third order FL, -ve and +ve FLs

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5
Q

What two ways can +ve FLs act?

A

Exponentially upwards OR downwards

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6
Q

The main example of a +ve FL is childbirth, the intial contractions cause stimulus to the stretch sensitive neurons in the cervix, what does this provoke and when does this stop?

A

Release of oxytocin (HM) from post PG to cause uterine muscles to contract more to help move baby towards cervix, this stops when stretch is lost

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7
Q

What is childbirth an example of?

A

NEuroendocrine reflex

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8
Q

What happens when there’s high blood sugar?

A

High - insulin gets released from islets of Lang + it binds to target cells, kinase cascade is activated, leads to exocytosis of GLUT4 channels for glucose uptake

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9
Q

What happens when there’s low blood sugar?

A

Low - glucagon released from islets of Lang, binds to target cells to promote glycogenolysis

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10
Q

What do cells do in response to adrenaline?

A

Vasoconstriction, insulin suppression, sensitisation of CNS and release of aas/NEFAs (energy source)

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11
Q

Why are responses to adrenaline beneficial?

A

Fight/flight

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12
Q

What triggers release of adrenaline?

A

Neuronal signal triggers adrenaline release from vesicles in medulla of adrenal gland to be released into blood

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13
Q

PNMT is produced in the adrenal gland, it converts noradrenaline to adrenaline but PNMT gene is only expressed when theres high levels of ??? present?

A

Glucocorticoids e.g. cortisol

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14
Q

All cells are capable of producing PNMT, what is the reason only cells in the adrenal gland do?

A

Area of high levels of glucocorticoids present in adrenal gland compared to elsewhere

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15
Q

What are neural crest cells?

A

They can act as neurons but are mobile towards particular signals

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16
Q

Some crest cells invade the middle of the adrenal gland during development and are responsible for adrenaline production (NA –> A), what are these cells called?

A

Chromaffin cells

17
Q

How do neural crest cells form during development?

A

The neural plate has borders (NPBs), the plate folds in at the NPBs to create the neural tube (eventually SC) and the cells from the borders migrate away as neural crest cells

18
Q

Chromaffin cells have cell bodies but no ??? so they are neurons that go nowhere

A

Axons

19
Q

How may you test if melatonin/cortisol are affecting sleep if either are?

A

Inject someone with both and compare effects or remove glands

20
Q

Which glands produce melatonin and cortisol?

A

Melatonin - pineal glands, cortisol - adrenal

21
Q

Melatonin and serotonin work in diurnal rhythm regulation, and the balance of the two regulates sleep, what may happen to night shift workers?

A

Insomnia due to severe disruption to diurnal cycles, peaks of melatonin can be decreased

22
Q

When looking at night shift workers diurnal cycles, what should be considered?

A

What job they do and stress coping mechanisms

23
Q

What does hyper-, hypo- and -mia mean?

A

Hyper - too much, hypo - too little, -mia - in the blood (hyperglycemia (too much glucose in the blood)

24
Q

Hormone and receptor need to be present to form a ??? and then a ??? elicits a target cell response

A

H-R complex, and activated H-R complex

25
Q

What happens when there is hormone resistance?

A

The target cell has a lack of response to the activated H-R complex

26
Q

What does it mean when a receptor is constitutively activated?

A

The target cell response is caused without the need for the ligand/HM

27
Q

Why must dosages of HM inhibitors be titrated?

A

Too much can switch from excess dosage to deficiency

28
Q
A