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Bio Module 5: communication, homeostasis and energy > Hormonal communication > Flashcards

Hormonal communication Flashcards

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1
Q

What’s the endocrine system?

A

A communication system that uses the blood to transport hormones (signalling molecules).

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2
Q

What’s a hormone?

A

A molecule released by endocrine glands directly into blood. They act as messengers carrying signals from gland to specific target cell or organ.

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3
Q

What’s a target cell?

A

For peptide hormones, cells that have complementary receptors on plasma membrane to hormone.

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4
Q

What are the 2 types of hormones?

A
  • protein, peptide and aa derivatives
  • steroid
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5
Q

Examples of peptide hormones

A

adrenaline, insulin, glucagon

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6
Q

Examples of steroid hormones

A

oestrogen, testosterone

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7
Q

Action of peptide hormones

A

Bind to receptor on plasma membrane of target cell and release a second messenger inside cell. Insoluble in phospholipid membrane.

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8
Q

Action of steroid hormones

A

Pass through membrane, enter cell and nucleus, have direct effect on DNA

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9
Q

What are endocrine glands?

A
  • ductless glands
  • group of cells that produce and release hormones directly into blood in capillaries surrounding the gland.
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10
Q

Examples of endocrine organs

A
  • pituitary
  • thyroid
  • thymus
  • adrenal
  • pancreas
  • ovaries
  • testes
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11
Q

How are signals detected?

A
  • hormones have a specific function and have an effect on one type of tissue only.
  • target cell receives endocrine signal.
  • peptide hormones bind to receptor (complementary) and initiate changes in the cell.
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12
Q

What’s the first messenger?

A

peptide hormones

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13
Q

What’s the second messenger?

A

cAMP

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14
Q

The action of first and second messengers

A

1) Hormone binds to receptor on plasma membrane which activates a transmembrane protein
2) G protein in membrane is then activated
3) G protein activates an effector molecule (usually an enzyme that converts an inactive molecule into the active second messenger)
4) effector molecule is adenyl cyclase which converts ATP to cAMP
5) cAMP may act directly on another protein, or it may initiate a cascade of enzyme controlled reactions that alter the activity of the cell.

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15
Q

What are the adrenal glands?

A
  • one pair of glands lying above the kidneys
  • outer layer - adrenal cortex
  • inner - adrenal medulla
  • both layers well supplied with blood vessel and secrete hormones directly into them.
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16
Q

What hormones are secreted by the adrenal glands (in order of part of gland they are released by) ?

A
  • aldosterone
  • cortisol
  • procursor molecules to sex hormones
  • adrenaline + noradrenaline (medulla)
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17
Q

Which hormone is secreted by the outermost layer of the adrenal cortex?

A

aldosterone

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18
Q

Which hormone is secreted by the middle layer of the adrenal cortex?

A

cortisol

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19
Q

What hormone is secreted by the innermost layer of the adrenal cortex?

A

thought to secrete precursor molecules that are used to make sex hormones

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20
Q

Where is the adrenal medulla?

A

centre of adrenal gland

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21
Q

What hormones are secreted by the adrenal medulla?

A
  • adrenaline
  • noradrenaline (also a neurotransmitter)
22
Q

How do (steroid) hormones secreted by the adrenal cortex have an effect on DNA?

A
  • Cholesterol used to produce steroid hormones which cause protein synthesis.

1) pass through plasma membrane of target cell
2) binds to receptor in cytoplasm
3) receptor - steroid complex enters the nucleus of target cell.
4) binds to another receptor on the chromosomal material
5) binding stimulates production of mRNA which code for production of proteins

23
Q

Action of aldosterone

A
  • helps control conc of Na+ and K+ in blood
  • Acts on cells in distal convoluted tubules + collecting ducts in kidneys
  • Increases absorption of Na+, decreases absorption of K+, and increases water retention which increases bp.
24
Q

Action of cortisol

A
  • released in response to stress or when blood glucose conc is low.
  • stimulates glycogenolysis in liver
25
Q

Function of adrenaline

A
  • increases stroke volume of the heart
  • stimulates glycogenolysis
  • relaxes smooth muscle of bronchioles
  • pupils dilate
  • vasoconstriction to raise bp
  • increases heart rate
26
Q

What are exocrine glands?

A

glands that secrete hormones into a duct

27
Q

How does the pancreas have both exocrine and endocrine functions.

A
  • secretes pancreatic juices containing enzymes into small intestine.
  • hormones secreted by islets of Langerhans into blood.
28
Q

What are acini?

A
  • tiny tubules surrounded by groups of exocrine cells
  • tubules join to form intralobular ducts that combine to form pancreatic duct (carries fluid into small intestines)
29
Q

What does the pancreatic duct contain

A
  • pancreatic amylase - digests amylose to maltose
  • lipase - digests lipids
  • trypsinogen - converted into active form (trypsin) when it enters the small intestine
  • sodium hydrogen carbonate - neutralise contents of the digestive system.
30
Q

Where are the islets of Langerhans?

A

in the lobules of acini

31
Q

Which cells make up the islets of Langerhans?

A
  • alpha cells that secrete glucagon
  • beta cells that secrete insulin
32
Q

How is insulin released?

A
  • released when blood glucose conc is too high
  • secretion must stop if it drops too low
    1) cell membranes of B cells contain Ca2+ and K+ ion channels.
    2) K+ ion channels are normally open but Ca2+ are normally closed. K+ diffuses out of cell making inside of the cell more -ve. At rest potential difference across cell membrane in -70mV.
    3) glucose moves into the cell when its conc is too high in blood by facilitated diffusion.
    4) glucose metabolised to ATP by glucokinase
    5) extra ATP causes K+ channels to close.
    6) K+ can’t diffuse out of cell and this alters the potential difference across the cell membrane, becomes less -ve inside
    7) this change in pot diff opens Ca 2+ ion channels
    8) Ca 2+ enter cell + cause secretion of insulin by making the vesicles containing insulin to move to the plasma membrane and fuse with it, releasing insulin by exocytosis.
33
Q

What’s hyperglycaemia?

A

when blood glucose conc rises too high for long periods, leads to organ damage.

34
Q

What’s hypoglycaemia?

A

When blood glucose conc drops and becomes too low for long periods. leads to inadequate delivery of glucose to tissues, brain in particular.

35
Q

Action of insulin on liver and muscle cells

A
  • high blood glucose conc detected by B cells in islets of Langerhans.
    1) insulin binds to specific receptor on membrane
    2) tyrosine kinase is activated
    3) tyrosine kinase causes the phosphorylation of inactive enzymes in cell, activating them leading to a cascade of enzyme controlled reactions inside the cell.
36
Q

Effects of insulin on cell

A
  • more transporter proteins specific to glucose placed into plasma membrane
  • more glucose enters
  • glycogenesis ( glucose —> glycogen)
  • more glucose converted into fats
  • more glucose used in respiration
37
Q

Action of glucagon

A
  • low blood glucose conc detected by a cells in islets of Langerhans that secrete glucagon
    1) glucagon binds to receptors, stimulating a G protein
    2) G protein activates adenyl cyclase
    3) adenyl cyclase converts ATP to cAMP
    4) this activates a series of enzyme controlled reactions in the cell
38
Q

Effects of glucagon

A
  • glycogenolysis (glycogen —> glucose)
  • more fatty acids used in respiration (conserves glucose)
  • a a and fats converted into additional glucose (gluconeogenesis)
39
Q

How is negative feedback involved in controlling blood glucose conc?

A
  • insulin and glucagon are antagonistic - have opposite effects on blood glucose conc
  • conc won’t remain constant, it will fluctuate around the optimum conc.
40
Q

What’s diabetes mellitus?

A
  • a condition in which blood glucose can’t be controlled effectively.
  • body can’t produce enough insulin leading to hyperglycaemia.
  • also hypoglycaemia as there’s no glycogen stores to convert to glucose when conc becomes too low in blood.
41
Q

Characteristics of Type 1 diabetes

A
  • usually starts in childhood
  • autoimmune disease - immune system destroys B cells so can’t produce insulin
  • may result from a viral attack
  • hyperglycaemia + hypoglycaemia
42
Q

Characteristics of Type 2 diabetes

A
  • can produce insulin but not enough
  • develops later in life
  • responsiveness to insulin decreases as you age
  • conc is almost permanently raised, damaging major organs + circulation
43
Q

Characteristics of both types of diabetes

A
  • can’t be cured
  • glucose present in urine
44
Q

How can type 1 diabetes be treated?

A
  • insulin pump therapy
  • insulin injection
  • islet cell transplant
  • pancreas transplant
45
Q

What’s insulin pump therapy

A

small device pumps insulin into blood through a needle that’s permanently inserted under skin.

46
Q

What’s islet cell transplantation?

A
  • healthy B cells of deceased donor implanted
  • may be possible to use stem cells to grow new islet of Langerhans. Freedom from daily insulin injections
47
Q

How can type 2 diabetes be treated?

A
  • changes in lifestyle - lose weight, exercise regularly and carefully monitor diet
  • medication that reduces amount of glucose released or boosts amount of insulin released by pancreas
  • in severe cases - insulin injections or drugs that slow down the absorption of glucose from the digestive system.
48
Q

Previous source of insulin

A

pancreas of animals (pigs)

49
Q

Current source of insulin

A

E. coli (bac) genetically modified to produce insulin.

50
Q

Advantages of using E. coli to produce insulin

A
  • exact copy of human insulin so faster acting + more effective and less chance of rejection due to an immune response.
  • lower risk of infection
  • people less likely to have moral objections

Bio Module 5: communication, homeostasis and energy (8 decks)

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