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Endocrine Key Information > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

three types of hormones

A
  1. protein and peptide
  2. steroid
  3. tyrosine derivatives
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2
Q

factors affecting the ability to measure hormones

A
  • pattern of secretion
  • presence of carrier proteins
  • interfering agents
  • stability of hormones
  • absolute concentrations (determined by rate of secretion)
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3
Q

response time of ligand-gated ion channels

A

milliseconds

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4
Q

what activates ligand-gated ion channels

A

neurotransmitters (substance can also be a hormone)

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5
Q

what does binding to a ligand-gated ion channel cause?

A

conformational change in the channel structure allowing influx/efflux of ions

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6
Q

example where a ligand-gated ion channel can go wrong

A

myasthenia gravis

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7
Q

example of a GPCR

A

adrenaline binding to beta2-adrenoceptors (lungs)

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8
Q

structure of GPCR

A

7 transmembrane spans coupled with G proteins

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9
Q

function of G proteins

A

stimulate/inhibit various types of effector molecules or ion channels

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10
Q

response time of GPCR

A

seconds due to enzyme activity and signal amplification

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11
Q

what does binding to a GPCR cause?

A

conformational change where the G-proteins dissociate

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12
Q

G-proteins in GPCR

A
  • alpha subunit
  • beta subunit
  • gamma subunit
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13
Q

explain the action of the alpha subunit in GPCR

A

GDP is exchanged with GTP when activated to give the protein energy to activate another substance.

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14
Q

structure of beta and gamma subunits

A

form a dimer

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15
Q

adrenaline bindings to alpha2-receptors?

A

K+ channels produces an inhibitory response (relaxation of the GI tract)

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16
Q

adrenaline biding to alpha-1-receptors causes?

A

vasoconstriction

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17
Q

signal amplification in GPCR

A
  • continual conversion of ATP to cAMP until switched off
  • increased number of enzymes activated and therefore responses
  • to switch off GTP must be hydrolysed on the alpha-subunit
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18
Q

what binds to receptor tyrosine kinases

A

hormones

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19
Q

response time of tyrosine kinases

A

hours

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20
Q

example of receptor tyrosine kinase

A

insulin

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21
Q

what does binding to receptor tyrosine kinase cause?

A
  • conformational change to the receptor so it becomes a dimer
  • autophosphorylation of tyrosine residues by ATP
  • relay proteins attach to residues which activates other proteins producing a divergent response
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22
Q

insulin actions produced by binding of the receptor tyrosine kinase

A
  • increased glucose transport channels
  • inhibition of gluconeogenesis
  • glycogen storage
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23
Q

three types of signalling

A
  1. autocrine
  2. paracrine
  3. endocrine
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24
Q

define autocrine

A

chemicals released bind to receptors on the cell that is releasing them

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25
Q

define paracrine

A

chemicals are released from the cells bind to receptors on adjacent cells

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26
Q

define endocrine signalling

A

chemicals are transported via the circulatory system to act on distant cells

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27
Q

two types of feedback

A
  1. negative: opposes change

2. positive: exaggerates change

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28
Q

actions of insulin

A
  • induces glucose uptake and utilisation by cells (muscle and liver)
  • promotes glycogenesis and lipogenesis
  • stimulate amino acid uptake and protein formation
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29
Q

define T2DM

A

state of insulin deficiency caused by resistance to insulin’s actions at target tissues, abnormal insulin secretion, inappropriate gluconeogensis and obesity (demand on pancreas).

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30
Q

aim of management in T2DM

A

optimise blood glucose

decrease risk of possible complications

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31
Q

non-pharmacological management of T2DM

A

lifestyle changes such as stop smoking, diet, body weight and exercise

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32
Q

two modes of action of pharmacological therapies in T2DM

A
  1. dependent upon insulin: increase secretion/decrease resistance and hepatic glucose output
  2. independent upon insulin: slowing absorption from GI tract/ enhancing excretion by kidney
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33
Q

insulin secretion in pancreatic beta cell

A
  • elevation of blood concentration leads to increased facilitated diffusion through GLUT2 into the beta cell
  • glucose phosphorylated by glucokinase
  • glycolysis of glucose-6-phosphate in mitochondria yields ATP
  • closure of ATP-sensitive K+ channels causes membrane depolarisation
  • opening of Ca2+ channels and intracellular Ca2+ triggers insulin release
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34
Q

what do SUs require

A

functional beta cells, efficacy can reduce with time

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35
Q

mechanism of action of SUs

A

displace ADP-Mg2+ from SUR1 closing KATP channels, stimulating glucose release

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36
Q

desirable effects of SUs

A

decrease fasting and post-prandial blood glucose

reduce long-term microvascular complications

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37
Q

short-acting SUs

A

tolbutamide

gliclazide

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38
Q

long-acting SUs

A

glibenclamide

glipizide

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39
Q

adverse of SUs

A
  • hypoglycaemia, increased risk in long-acting agents, elderly, reduce hepatic/renal function (CKD)
  • weight gain due to anabolic effect of insulin and appetite increased and urinary loss of glucose decreased
40
Q

when are SUs used?

A

first line if intolerant to metformin or with weight loss

41
Q

which drugs decrease the action of SUs

A

thiazide diuretics

corticosteroids

42
Q

examples of glinides

A

repaglinide and nateglinide

43
Q

glinides mechanism of action

A

increased by glycaemia

- bind to SUR1 (benzamido site) to close KATP channels and trigger insulin release

44
Q

how are SUs delivered and peak action time?

A

oral

1-2 hours

45
Q

how are glinides delivered

A

orally

46
Q

onset of glinides

A

rapid onset (30-60 minutes) and offset (4hours), response to meals

47
Q

desirable effects of glinides

A
  • reduce post-prandial blood glucose concentration

- less likely to cause hypoglycaemia

48
Q

when are glinides used?

A

in conjunction with metformin and TZDs

49
Q

why is repaglinide favoured?

A

mainly hepatic metabolism and therefore is safer in CKD

50
Q

when are glinides not used

A

hepatic impairment, pregnancy or breast feeding

51
Q

define the incretin effect

A

insulin responses greater to oral glucose than IV

52
Q

response to oral glucose (incretins)

A
  • ingestion of food stimulates release of GLP-1 and GIP from enteroendocrine cells
  • GLP-1 and GIP enter the portal blood
  • enhance insulin release from beta cells and delay gastric emptying
  • GLP-1 decreases glucagon release from alpha cells and decreases glucose production
  • end result is decreased blood glucose
53
Q

examples of DPP-4i

A

sitagliptin, saxagliptin, vildagliptin, linagliptin and alogliptin

54
Q

the incretin effect is impaired in T2DM but can be restored by

A
  • reducing breakdown of endogenous incretins

- administering exogenous incretins resistant to breakdown

55
Q

what terminates the actions of GLP-1 and GIP

A

enzyme dipeptidyl peptidase-4 within minutes

56
Q

what competitively inhibits DPP-4

A

gliptins/DPP4i

57
Q

when are DPP4i used?

A

combination with metformin or SU, but can be used as a monotherapy

58
Q

adverse of DPP4i

A

nausea

59
Q

examples of incretin analogues

A

extenatide

liraglutide

60
Q

mechanism of action of incretin analogues

A
  • mimic the action of GLP-1 but resist breakdown by DPP-4. agonists of GPCR GLP-1 the increase intracellular cAMP stimulating insulin release
  • also suppress glucagon, slow gastric emptying and decrease appetite
61
Q

desirable effects of incretin analogues

A

weight loss

reduce hepatic fat accumulation

62
Q

how are incretin analogues administered

A

SC

63
Q

adverse of incretin analogues

A

nausea

pancreatitis

64
Q

describe alpha glucosidase

A

brush border enzyme that breaks down starch and disaccharides to glucose (glycogenolysis)

65
Q

alpha glucosidase inhibitors examples

A

acarbose
miglitol
voglibose

66
Q

how are alpha glucosidase inhibitors taken

A

with a meal to delay absorption of glucose and reduce postprandial increase in blood glucose

67
Q

when are alpha glucosidase inhibitors used

A

T2DM that are inadequately controlled by lifestyle and other drugs
infrequently used in the UK

68
Q

adverse of alpha glucosidase inhibitors

A

flatulence
loose stools
diarrhoea

69
Q

example of biguanides

A

metformin

70
Q

when is metformin first line?

A

T2DM irrespective of obesity with normal hepatic and renal function

71
Q

mechanism of action of metformin

A

reducing hepatic gluconeogenesis by stimulating AMP-activated protein kinase (AMPK), increasing glucose uptake and utilisation by skeletal muscle (increasing insulin signalling), reducing carb absorption and increasing fatty acid oxidation

72
Q

desirable effects of metformin

A
  • reduces microvascular complications
  • administered orally and can be combined with other agents e.g. insulin, TZDs and SUs
  • prevents hyperglycaemia, but doesn’t cause hypoglycaemia
  • weight loss
73
Q

adverse of metformin

A

GI upset and lactic acidosis (hepatic/ renal disease and excess alcohol)

74
Q

describe thiazolidinediones (TZDs)

A

enhance insulin action at target tissues, without affecting insulin secretion (reduce insulin resistance)

75
Q

mechanism of action of TZDs

A
  • exogenous agonists of PPAR-gamma (nuclear receptor) which associates with RXR
  • largely confined to adipocytes
  • activated complexes act as transcription factors promoting expression of genes encoding several proteins involved in insulin signalling and lipid metabolism
76
Q

desirable effects of TZDs

A
  • promote fatty acid uptake and storage in adipocytes, rather than in skeletal muscle and liver
  • reduce hepatic glucose output
  • enhance peripheral glucose uptake and do not cause hypoglycaemia
77
Q

adverse of TZDs

A
  • weight gain (differentiation of pre-adipocytes contributes)
  • fluid retention (promotes Na+ reabsorption by the kidney)
78
Q

examples of TZDs

A

ciglitzon
troglitzone
pioglitzone

79
Q

why are some TZDs no longer used?

A

cause serious hepatotoxicity

80
Q

which is the only TZD used?

A

pioglitzone in combination with metformin or SUs

81
Q

mechanism of action of SGLT2i

A

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

82
Q

desirable effect of SGLT2i

A

calorific loss and water accompanying glucose (osmotic diuresis) contributes to weight loss

83
Q

examples of SGLT2i

A

dapaliflozin
canagliflozin
empagliflozin

84
Q

three ways the hypothalamus integrates endocrine and nervous system

A
  1. secretion of regulatory hormones which control activity of anterior pituitary cells
  2. synthesises hormones and transports them to the posterior pituitary via infundibulum
  3. direct neural control (NA and adrenaline by adrenal medulla)
85
Q

diurnal contort of hormone levels

A
  1. external cues (light/dark)

2. hormone levels influenced by rate of elimination from the body

86
Q

describe steroid hormones

A

lipids derived from cholesterol, secreted not stored

87
Q

transport of steroid hormones

A

hydrophobic and transported in blood plasma binding to carrier proteins
pass through the plasma membrane forming an activated hormone-receptor complex which binds to DNA and activates specific genes to produce specific proteins

88
Q

when are steroid hormones biologically active

A

when they are unbound

89
Q

two types of amine hormones

A
  1. catecholamines

2. thyroid amines

90
Q

how are catecholamines transported

A

hydrophilic, unbound in plasma

91
Q

how are thyroid amines transported

A

bound to carrier proteins

92
Q

amine hormones storage

A

stored as vesicles until needed to bind to membrane bound receptors and evoke cellular responses

93
Q

examples of peptide and protein hormones

A

oxytocin and ADH

GH and insulin

94
Q

how are peptide and protein hormones transported

A

hydrophilic and transported unbound in blood plasma

95
Q

synthesis of protein and peptide hormones

A

synthesised as precursor molecules and stored in secretory vesicles
cleaved by enzymes

96
Q

binding to carrier proteins provides the following effects

A
  • facilitation of hormone transport
  • increased half-life of hormone
  • reservoir of hormone
97
Q

specific carrier proteins

A

cortisol-binding globulin
thyroxine-binding globulin
sex steroid-binding globulin

Endocrine Key Information (2 decks)

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