Physiology Flashcards

1
Q

Of endocrine and exocrine glands, which enter into bloodstream and which have ducts?

A

Endocrine = ductless, enter bloodstream Exocrine = ducts (doesnt enter systemic circulation)

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2
Q

How is specificity of signalling achieved in the endocrine system?

A

1) Chemically distinct hormones 2) Specific receptors for each hormone 3) Distinct distribution of receptors across target cells

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3
Q

What are the 7 ‘classic’ endocrine glands?

A

Pituitary, Thyroid, parathyroid, adrenals, pancreas and ovaries/testes

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4
Q

What are the 4 main chemical natures of hormones, with examples

A

1) Modified amino acids (A) e.g. adrenaline/thyroid hormones 2) Steroids (S) eg. cortisol 3) Peptides (P) eg. ADH 4) Proteins (P) eg. insulin

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5
Q

Do hormones act at low or high concentrations and at low or high potency?

A

Hormones act at low concentration over large distances to activate specific receptors with high potency.

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6
Q

Are hormone slower/longer or faster/shorter than neurotransmitters?

A

Slower and more enduring

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7
Q

How is action of hormones terminated?

A

Enzyme-Mediated metabolic inactivation (in liver or at site of action)

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8
Q

What are amine hormones synthesised from?

A

Amino acids eg. tyrosine -> adrenaline

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9
Q

What stimulates amines and protein/peptide hormones to be released into systemic circulation?

A

Ca2+ dependent exocytosis

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10
Q

What are peptide and protein hormones synthesised from?

A

Longer precursors eg. polypeptides before being snipped/modified by converses

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11
Q

How do steroids differ from other types of hormones in terms of synthesis and secretion?

A

They are made on demand, so aren’t stored in vesicles like other hormones. They also are lipophilic so require transport proteins to travel in circulation, while others are released directly

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12
Q

How are all steroid hormones synthesised?

A

Biosynthetic pathway via pregnenolone

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13
Q

Which hormones require transport/carrier proteins?

A

Steroids, thyroxine (T4) and triiodothyronine (T3)

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14
Q

Which specific carrier protein binds cortisol?

A

Cortisol-binding globulin (CBG)

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15
Q

Which specific carrier protein bind testosterone and oestradiol?

A

Sex steroid-binding globulin (SSBG)

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16
Q

What are 2 important general carrier proteins?

A

Albumin and transthyretin

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17
Q

What is neuroendocrine control?

A

A sudden burst in secretion to meet a specific stimulus e.g.. in response to stress

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18
Q

What are the 3 main control systems for hormone secretion?

A

Negative feedback, neuroendocrine and diurnal rhythm

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19
Q

What are the 3 main types of hormone receptors?

A

G-Protein Coupled (GPCR), receptor kinases and nuclear receptors

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20
Q

Of the 3 main types of hormone receptors, which are cell surface and which are intracellular?

A

GPCRs and receptor kinases are cell surface. Nuclear receptors are intracellular

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21
Q

What are the 3 sub-divisions of nuclear receptors?

A

Class 1 (mainly steroids), Class 2 (mostly lipids) and Hybrid class (e.g. T3)

22
Q

What are normal blood glucose levels?

A

5mM (should not be >11mM)

23
Q

When is insulin released?

A

Post-feeding when blood glucose levels rise

24
Q

When is glucagon released?

A

Post-starvation when blood glucose levels drop

25
Q

What are the endocrine cells of the pancreas?

A

Islets of Langerhans

26
Q

What do β cells secrete?

A

Insulin

27
Q

What do α cells secrete?

A

Glucagon

28
Q

What do δ cells secrete?

A

Somatostatin

29
Q

What do α cells secrete?

A

Pancreatic polypeptide

30
Q

What is insulin synthesised from?

A

Larger single chain preprohormone, preproinsulin, then cleaved into proinsulin and a signal peptide, then cleaved into insulin and C-peptide

31
Q

Is insulin lispro ultrafast or ultra long acting?

A

Ultra fast

32
Q

Is insulin glargine ultrafast or ultra long acting?

A

Ultra long

33
Q

How does glucose enter the β cells for the secretion of insulin, and what happens to it?

A

Glucose enters β cells through the GLUT2 glucose transporter and is phosphorylated by glucokinase

34
Q

How does phosphorylation of glucose cause the secretion of insulin from the β cells?

A
  1. Increased metabolism of glucose leads to an increase in intracellular ATP concentration
  2. ATP inhibits the ATP-sensitive K+ channel KATP, resulting in the build up of K+ inside the cell.
  3. This leads to depolarisation of the cell membrane, opening of voltage-gated Ca2+ channels
  4. An increase in internal Ca2+ concentration leads to fusion of secretory vesicles with the cell membrane and release of insulin
35
Q

What acts as a glucose sensor?

A

Glucokinase

36
Q

True or False, release of insulin is biphasic

A

True

37
Q

What can mutations in Kir6.2 and SUR1 in humans lead to?

A

Neonatal diabetes and congenital hyperinsulinism

38
Q

What mutations can cause Maturity-onset diabetes of the young (MODY)?

A

Mutations of at least 6 different genes involved in beta-cell function can cause it: glucokinase, and several transcription factors, including hepatocyte nuclear factor

39
Q

What kind of receptor is the insulin receptor?

A

A dimeric tyrosine kinase

40
Q

What is Donohue syndrome and how does it relate to diabetes

A

Leprechaunism - rare autosomal recessive genetic trait. Causes severe insulin resistance

41
Q

What is insulin resistance?

A

The reduced ability to respond to ‘physiological’ insulin levels, and is thought to occur primarily through reduced insulin sensing and/or signalling.

42
Q

What is Rabson Mendenhall Syndrome?

A

Rare autosomal recessive genetic trait resulting in severe insulin resistance, hyperglycemia and compensatory hyperinsulinemia

43
Q

Where and how are ketone bodies formed?

A

Liver mitochondria, derived from acetyl-CoA from beta-oxidation. - They diffuse into the blood stream and to peripheral tissues and are important molecules of energy metabolism

44
Q

Why are ketone bodies formed in starvation and diabetes?

A

When glucose is not available, oxaloacetate is consumed for gluconeogenesis as an alternative. This results in excess acetyl-CoA as part of the pathway, resulting in excess ketone bodies

45
Q

Is ketoacidosis associated with Type 1, Type 2 or both types of diabetes?

A

Just Type 1 usually

46
Q

What is the structure of the KATP channel?

A

Octomeric complex of 4x 6.2 subunits (Kir6.2) formign the potassium inward rectifier channel, and four sulphonylurea receptor 1 subunits (SUR1)

47
Q

What causes the KATP channel to close (structurally)?

A

ATP binding to each of the Kir6.2 subunits closes the channel causing depolarization of the b cell and insulin release

48
Q

What causes the KATP channel to open (structurally)?

A

ADP-Mg2+ binding to the SUR1 subunits opens the channel maintaining the resting potential of the b cell and inhibits insulin secretion (when extracellular glucose is low)

49
Q

What is the main type of receptor for sensing the internal environemnt?

A

G-Protein Coupled Receptors

50
Q

What kind of hormone receptor is the insulin receptor?

A

Tyrosine kinase receptor

51
Q
A