Hormonal Communication Flashcards

1
Q

The endocrine communication system uses hormones as signalling molecules: what is the process of this system

A
  1. Secretion (production & release) of hormones into the bloodstream
  2. Hormones transported by blood
  3. Hormone detected by target cells / tissues / organs
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2
Q

How do endocrine hormones move vs exocrine ones

A

Secreted directly into the blood versus secreted via a duct

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3
Q

What are the 2 types of hormones

A

Protein (non steroid) & steroid

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4
Q

Protein (non-steroid hormones) Vs Steroid hormones

A
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5
Q

How do hormones work on target cells / tissues

A
  • specific receptor on cell-surface membrane
    (Receptor made of glycoproteins)
    -> complementary to shape of hormone molecule
    -> hormone binds to receptor & changes initiated in the cells
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6
Q

1st vs 2nd messenger

A
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7
Q

How is the second messenger activated process

A
  1. 1st non steroid messenger binds to receptor on cell surface membrane
  2. G protein activated
  3. Adenyl cyclase - effector molecule - activated
  4. ATP converted to cAMP (2nd messenger)
  5. cAMP acts directly on another protein (e.g, ion channel) or may initiate a cascade of enzyme controlled reactions, which alter cell activity
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8
Q

What organ functions as an endocrine and exocrine gland

A

The pancreas

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9
Q

Exocrine function of pancreas

A

-> secrete pancreatic juices into pancreatic duct (delivered to small intestine)

Pancreas juices made up of
- digestive enzymes (amylase, trypsin, lipase)
- sodium hydrogencarbonate (neutralises contents of digestive system, which has left the acidic stomach)

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10
Q

Endocrine function of pancreas

A
  • secrete hormones from the islets of langerhans
    + endocrine tissues are made up of these islets
    -> alpha & beta cells are found in these island
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11
Q

Alpha vs beta cells in pancreas

A
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12
Q

Key processes in Pancreas (glycogenolysis, glycogenesis, gluconeogenesis, lipogenesis)

A
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13
Q

What does glucagon do

A
  • stimulate glycogenolysis
  • stimulate gluconeogenesis
    # released if blood glucose concentration too low
    -> glucose conc in blood increases, as glucose conc in cell e.g. muscles / hepatocytes increases
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14
Q

What does insulin do

A
  • released if blood glucose too high
  • stimulates glycogenesis
    -glucose concentration of cells e.g. muscles / hepatocytes decreases therefore in blood decreases
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15
Q

What mechanism regulates blood glucose conc (normally 4-6 mol/dm3)

A

Negative feedback
This is as it’s insulin versus glucagon (antagonistic as they have the opposite effects)

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16
Q

What happens in hypoglycaemia & how is it detected (when too low blood glucose conc)

A

When not enough glucose is delivered to the body tissues & brain
This can lead to seizures, unconsciousness / death

-> detected in alpha cells in the islet of langerhans
Glucagon is secreted into bloodstream
Receptors on the outside of hepatocytes & muscle cells detect glucagon
-> activates gluconeogenesis, glycogenolysis & decreased rate of respiration
-> concentration of glucose in cells increases and so concentration of glucose in blood increases as glucose diffuses into blood from cells

17
Q

What happens in hyperglycaemia& how is it detected (when too high blood glucose conc)

A

-> detected by beta cells in the islet of langerhans
- insulin secreted into the bloodstream!
- receptors on outside of hepatocytes & muscle cells detect insulin
- activates glycogenesis & increased rate of respiration & lipogenesis

Glucose concentrate decreases in cells & blood as glucose diffuses into cells from blood, down the concentration gradient by facilitated diffusion

18
Q

Mechanism of insulin secretion

A
19
Q

What ion channels are open & closed @ a normal blood glucose level

A
  • ca2+ closed
  • K+ open
20
Q

How is insulin secrete when BGC is high (steps)

A
  1. Glucose molecules move into the beta cells by a glucose transported
  2. Glucose metabolised in mitochondria via glucokinase to form ATP
  3. Extra ATP binds to K+ channels & causes their closure
  4. K+ can’t diffuse out of cell / builds up / inside less negative / P.D reduced / depolarised membrane
  5. Voltage gated Ca2+ ion channels open
  6. Ca2+ enter cells
  7. Secretion of insulin (vesicles contains it move towards & fuse with the cell surface membrane)
  8. Insulin released by Exocytosis
21
Q

Insulin action in hepatocytes

A
22
Q

Glucagon action to do with hepatocytes

A
23
Q

Type 1 diabetes (insulin dependent) cause
& typical onset

A
  • in childhood
    Cause = autoimmune response or viral infection, in which the immune system destroys beta cells OR physical trauma
24
Q

Type 1 diabetes symptoms

A

Weight loss (less glucose converted into glygogen, lipids etc & stored - lost in urine instead)
More urine produced (less water reabsorbed in the collecting duct, due to high glucose conc

25
Q

Effects of type 1 diabetes on the body

A
  • insulin can no longer be synthesised by beta cells in the pancreas to control blood glucose concentration
  • excess glucose can’t be stored as glycogen
  • excess glucose not removed quickly: prolonged periods of high b.g.c. especially after meals
    -> no store of glycogen, which can be used to release glucose -> blood g.c. falls too low
26
Q

Type 1 diabetes: typical treatment vs in severe cases vs potential treatments

A
27
Q

Type 2 diabetes (non-insulin dependent) onset & causes?

A

Over 40, but many children getting it now

Beta cells still produce insulin, but it’s ineffective
-> specific receptors on cell surface membrane of liver & muscle cells = less responsive to it
- cells lose ability to respond to insulin in blood

28
Q

Risk factors for type 2 diabetes

A
  • obesity
  • lack of regular exercise
  • high blood pressure & cholesterol
  • ethnicity (Asian & Afro-Caribbean)
  • family history
29
Q

Type 2 diabetes: typical vs severe treatment

A
30
Q

Alternate insulin sources & evaluation of them?

A
  1. Pig Insulin ( 🐷 pancreas = matches human close, but some = ethical or religious objections)
  2. Genetically modified bacteria producing insulin
31
Q

Adrenal glands structure

A
32
Q

What does the adrenal cortex secrete

A

Mineralcorticoids like aldosterone
Glucocorticoids like cortisol
- precursor androgen molecules, which are used to make sex hormones like testosterone & oestrogen

33
Q

What does aldosterone regulate

A

Levels of sodium & potassium & water balance in blood, which impacts blood volume & pressure by targeting the collecting duct

34
Q

What does cortisol, the primary stress hormone regulate

A

Released in response to stress & low B.G.C
-> regulates metabolism of glucose, fats & proteins -> releasing usable energy
-> stimulates production of glucose from stored compounds: glycogen, fats & proteins in the lvier

35
Q

What do sex hormones do

A

Help development of secondary sexual characteristics & regulate production of gametes

36
Q

What does the adrenal medulla secrete

A
  • adrenaline & noradrenaline
37
Q

Effects of adrenaline

A

Increases breathing rate not heart rate

38
Q

Effects of noradrenaline

A
  • works with adrenaline in response to stress
    Increases heart rate
    Widens pupils
    Widens air passages in lungs
    Narrow blood vessels in non-essential organs (so higher blood pressure)
39
Q

When is adrenaline produced & how does it work

A

Produced @ times of stress of excitement: prepares the body for activity & to respond to emergency situations (fight/flight)
-> binds to specialised adrenaline receptors on cell-surface membrane of target cells (many cells & tissues have adrenaline receptors)