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Endocrine SB > Pharmacology and Physiology > Flashcards

Pharmacology and Physiology Flashcards

1
Q

what type of glands are endocrine glands

A

ductless

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2
Q

what are the 3 types of chemical signalling

A

autocrine - cell acting on itself
paracrine - local activity, secrete into surrounding tissue
endocrine - works on distant tissue

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3
Q

what are the 3 main classes of hormones

A

(Glyco)proteins and peptides
Steroids
Tyrosine and tryptophan derivatives

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4
Q

what are (glyco)proteins and peptides made of and example

A

amino acid chains of variable length

e.g. insulin

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5
Q

what are steroids made from and example

A

cholesterol

e.g. cortisol, testosterone

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6
Q

examples of Tyrosine and tryptophan derivatives

A

adrenaline

thyroid hormones

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7
Q

how are amines synthesised, stored, released and transported

A

pre-synthesised, stored in vesicles, released in response to stimuli by Ca2+-dependent exocytosis

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8
Q

how do amines and peptide/proteins travel in the blood

A

are hydrophilic

transported mainly free in plasma

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9
Q

how are peptides/proteins synthesised, stored, released and transported

A

pre-synthesised usually from a longer precursor, stored in vesicles, released in response to stimuli by Ca2+-dependent exocytosis

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10
Q

where are precursor proteins synthesised

A

at ribosomes of rough ER

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11
Q

how are steroids synthesised, stored, released and transported

A 
synthesised and secreted upon demand. 
Stimuli increase (i) cellular uptake and availability of cholesterol (ii) rate of conversion of cholesterol to pregnenolone (rate limiting step)
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12
Q

what is the RLS in steroid conversion

A

conversion of cholesterol to pregnenolone

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13
Q

what is the storage of steroids

A

is no storage

are made then immediately secreted

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14
Q

how do steroids travel in the blood

A

are hydrophobic
transported mainly bound
only ‘free’ if biologically active

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15
Q

what is the role of carrier proteins

A

(i) increase amount of hormone transported in blood

(ii) prevent rapid excretion by preventing filtration at the kidney

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16
Q

important specific carrier proteins

A

Cortisol-binding globulin (CBG)
Thyroxine-binding globulin (TBG)
Sex steroid-binding globulin (SSBG)

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17
Q

important general carrier proteins

A

Albumin – binds many steroids and thyroxine

Transthyretin – binds thyroxine and some steroids

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18
Q

why do proteins and peptide not require a carrier protein

A

as they are soluble in plasma

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19
Q

why do steroids and thyroxine require a carrier protein

A

as they are insoluble

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20
Q

what is the role of CBG, TBG and SSBG

A

CBG - binds cortisol in a selective manner (also some aldosterone)
TBG - binds thyroxine (T4) selectively (also some triiodothyronine (T3)
SBBG - binds mainly testosterone and estradiol

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21
Q

what is relationship of free and bound hormones and what helps regulate this

A

in equilibrium

carrier proteins

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22
Q

what hormones can cross the capillary wall

A

only free hormones

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23
Q

what is primary determinant of plasma concentration

A

rate of secretion

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24
Q

what are the ways to control hormone levels

A

1 - negative feedback
2 - neuroendocrine - sudden burst in secretion to meet a specific stimulus
3 - diurnal/circadian rhythm - secretion rate fluctuates (up and down) as a function of time

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25
Q

what are the different types of hormone receptors

A
  • G-protein coupled receptors
  • Receptor kinases
  • Nuclear receptors
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26
Q

what are the classes of nuclear receptors

A

Class 1 - activated by many steroid hormones. Mainly located in the cytoplasm bound to heat shock proteins. Move to nucleus when activated

Class 2 - activated mostly by lipids, found in the nucleus

Hybrid Class - activated by thyroid hormone (T3). Similar to Class 1.

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27
Q

how signalling via receptor kinases works, using insulin as an example

A

1 -unbound
2 - insulin binds
3 - Binding of insulin causes autophosphorylation of intracellular tyrosine residues
4 - Recruitment of multiple adapter proteins, notably IRS1, that are also tyrosine phosphorylated
5 - insulin receptor substate proteins
6 - cellular effects

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28
Q

signalling bia nuclear receptors class 1

A

1 - steroid hormones enter cell by diffusion across plasma membrane
2 - combine with intracellular receptor
3 - produce HSP
4 - receptor-steroid complex moves from cytoplasm to nucleus
5 - forms a dimer
6 - binds to hormone response elements in DNA
7 - transcription of specific genes is either ‘switched-on’ (transactivated) or ‘switched off’ (transrepressed)
8 - mRNA levels altered
9 - rate of synthesis of mediator proteins altered

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29
Q

what is the only biguanide used in diabetes

A

Metformin

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30
Q

what is the function of Metformin

A

Insulin sensitiser

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31
Q

usual starting dose for metformin

A

500mg twice a day

32
Q

overall effects of Metformin

A

Hyperglycaemia management:
Reduces HbA1c by 15-20mmol/mol by lowering insulin resistance

Hypoglycaemia:
Does not cause hypos when used as monotherapy

Weight Effect:
Overall weight neutral but sometimes can reduce weight

Prevention of microvascular and macrovascular complications

33
Q

What are the additional effects of Metformin

A 
Reduces triglycerides and LDL - improves lipid profiles 
Safe in pregnancy
- Gestational DM
- Pre-existing T2DM
Polycystic ovarian syndrome (PCOS)
NAFLD
34
Q

Metformin side effects

A

GI side effects:
Anorexia, nausea, vomiting, diarrhoea, abdo pain, taste disturbance

Lactic Acidosis
Liver failure
Rash

35
Q

MOI of Metformin

A

Reduces hepatic gluoconeogenesis [by stimulating AMP-activated protein kinase (AMPK)]
Increases glucose uptake and utilization by skeletal muscle (increases insulin signalling)

36
Q

what are sulphonylureas, give 2 examples

A

Insulin Secretagogues

  • Glicazide
  • Glipizide
37
Q

SU’s effects

A

Hyperglycaemia management:
Reduces HbA1c by 15-20 mmol/mol by increasing insulin secretion

Prevention of Microvascular complications

38
Q

SUs side effects

A

Hypoglycamia
Weight gain
GI upset - headache
Avoid in severe renal or hepatic failure

39
Q

MOI of SU

A
  • Displacing the binding of ADP-Mg2+ from the SUR1 subunit

- Thus closing the KATP channel and stimulating insulin release

40
Q

what is Thiazolidinediones (TZD) and what is the only agent available

A

PPARgamma agonists

- Pioglitazone

41
Q

TZDs effects

A

Hyperglycaemia:
Reduces HbA1c by 15-20mmol/mol by increasing insulin sensitivity

Promote fatty acid uptake and storage in adipocytes, rather than skeletal muscle and liver
Reduced hepatic glucose output

Can cause fluid retention in HF
But reduces risk of MI

42
Q

Function of TZDs

A

Enhance the action of insulin at target tissues, but do not directly affect insulin secretion – reduce the amount of insulin required to maintain a given blood level of glucose

43
Q

MOI of TZDs

A
  • exogenous agonists of the nuclear receptor PPARγ which associates with retinoid receptor X (RXR)
  • Activated PPARγ-RXR complex acts as a transcription factor that binds to DNA to promote the expression of genes encoding several proteins involved in insulin signalling
44
Q

what are the proteins involved in insulin signalling

A

Lipoprotein lipase
Fatty acid transport protein
GLUT4

45
Q

Side effects of TZDs

A

Weight gain

Fluid retention

46
Q

what are incretins

A

Intestinal Secretion of Insulin

47
Q

examples of incretins

A

GIP from K cells
GLP-1 from L cells
(cells in the small intestines)

48
Q

what do GLP-1 and GIP do

A

enhance (increment) insulin release from pancreatic β-cells (and delay gastric emptying)

49
Q

what does GLP-1 do also

A

decreases glucagon release from pancreatic α-cells

50
Q

what do these actions by GLP-1 and GIP lead to

A

enhanced glucose uptake and utlization
+ decreased glucose production

= decreased blood glucose

51
Q

what is Exenatide and what dose is given

A

GLP-1 Receptor Agonists

subcutaneously twice daily

52
Q

MOI of Exenatide

A
  • Binds to GPCR GLP-1 receptors that increase intracellular cAMP concentration
  • Increases insulin secretion, suppresses glucagon secretion, slows gastric emptying, decreases appetite
53
Q

Effects of Exenatide

A

Promote insulin secretion from pancreas without hypoglycaemia

Suppress glucagon (which is increased in T2DM)

Decrease gastric emptying – early satiety

Modest weight loss (reduced appetite)

Reduces hepatic fat accumulation

54
Q

Side effects of Exenatide

A

Nausea

Pancreatitis

55
Q

what GLP-1 Agonist can be given once daily

A

Liraglutide

56
Q

how is the actions of GLP-1 and GIP terminated

A

rapidly by the enzyme DPP-4

57
Q

what are Gliptins and what is there function

A

DPP-4 inhibitors

prolong the actin of GLP-1 and GIP

58
Q

what are the benefits of DPP-4 inhibitors

A

Promote insulin secretion from pancreas without hypoglycaemia

Suppress glucagon (which is increased in T2DM)

Weight neutral

59
Q

example of DPP-4 inhibitors

A

Sitagliptin

60
Q

why are SGLT2 inhibitors different from other treatments

A

do not rely on insulin

61
Q

MOI of SGLT2 inhibitors

A

selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney nephron to deliberately cause glucosuria

62
Q

how does SGLT2 inhibitors get rid of the glucose

A

pee out the glucose

decrease uptake of sugar by roughly 1/4

63
Q

positive affects of SGLT2 inhibitors

A

decrease in blood glucose with little risk of hypoglycaemia

weight loss- Calorific loss and water accompanying glucose

64
Q

side effects of SGLT2 inhibitors

A

sugar in urine

- increase in thrush and UTIs

65
Q

example of SGLT 2 inhibitor

A

dapagliflozin

66
Q

how is the Katp channel opened and closed

A

closed - ATP binding to Kir6.2 subunits causing depolarisation. Insulin released.

open - ADP-Mg2+ binding to the SUR1 subunits maintaining the resting potential. Insulin not released

67
Q

how do SUs work

A

bind to SUR1 and close the Katp channel causing depolarisation
and insulin release

68
Q

what are the parts of the Katp channel

A

Kir6.2

SUR1

69
Q

what are Glinides

A

Act similarly to the sulfonylureas – bind to SUR1 (at a distinct benzamido site) to close the KATP channel and trigger insulin release

70
Q

examples of Glinides

A

repaglinide

nateglinide

71
Q

why are Glinides used sometimes over SUs

A

Have rapid onset/offset kinetics – less likely to cause hypoglycaemia than sulfonylureas

72
Q

what is alpha-glucosidase

A

brush border enzyme that breaks down starch and disaccharides to absorbable glucose

73
Q

what do Inhibitors of α-glucosidase do

A

delay absorption of glucose thus reducing postprandial increase in blood glucose

74
Q

when are Inhibitors of α-glucosidase used

A

in 2TDM patients inadequately controlled by life style measures or other drugs

75
Q

what is an example of Inhibitors of α-glucosidase

A

Acarbose

76
Q

side effects of Inhibitors of α-glucosidase

A

GI upset - loose stools, diarrhoea, abdominal pain, bloating

77
Q

why are Inhibitors of α-glucosidase useful

A

pose no risk of hypoglycaemia

Endocrine SB (15 decks)

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