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Endocrine: Basic Science > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

examples of steroid hormones

A

cortisol

testosterone

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2
Q

examples of tyrosine derivative hormones

A

thyroxine

epinephrine

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3
Q

what does the ability to measure hormones depend on?

A 
pattern of secretion
presence of carrier proteins
interfering agents
stability of hormone
absolute concentrations (determined by rate of secretion)
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4
Q

four types of membrane-bound receptors

A

ligand-gated ion channels
GPCR
receptor tyrosine kinase (kinase-linked receptors)
steroid hormone receptors

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5
Q

response time of ligand-gated ion channels

A

milliseconds

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6
Q

describe how ligand-gated ion channels work?

A
  • activated by neurotransmitters (can also be hormones)

- binding causes conformational change in channel structures allowing influx/efflux of ions

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7
Q

example when membrane bound ion channel goes wrong?

A

myasthenic gravis

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8
Q

examples of GPCR

A
  • adrenaline binding to beta2-adrenoceptors in the lungs
  • adrenaline binding to alpha2-receptors leading to inhibition in the GI tract (K+ channels)
  • adrenaline to alpha1-receptors causes vasoconstriction
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9
Q

structure of GPCR

A

7 transmembrane spans across the cell membrane coupled with G-proteins that 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 a GPCR do?

A

binding causes conformation change where the G-proteins dissociate

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12
Q

three G-proteins

A

alpha subunit

beta and gamma subunits

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13
Q

role of the alpha subunit?

A

GDP is attached and is exchanged with GTP to give the protein energy to activate another substance.
to stop this the GTP must be hydrolysed

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14
Q

what do the beta and gamma subunits do?

A

form a dimer

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15
Q

describe signal amplification in GPCR

A
  • continual conversion of ATP to cAMP until switched off
  • increased number of enzymes activated and therefore responses
  • switched off by GTP hydrolysis
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16
Q

what binds to receptor tyrosine kinases?

A

hormones e.g. insulin

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17
Q

how long do receptor tyrosine kinases take to act?

A

hours

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18
Q

describe how receptor tyrosine kinases work?

A
  • binding causes conformational change to the receptor which becomes a dimer
  • autophosphorylation of tyrosine residues by ATP and relay proteins attach to residues which activates other proteins producing a divergent response
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19
Q

explain how the hormone insulin binding produces a divergent response?

A

produces a variety of responses:

  • glucose transport channels
  • inhibition of gluconeogenesis
  • glycogen storage
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20
Q

examples of substances that bind to steroid hormone receptors

A

glucocorticoids

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21
Q

describe how steroid hormone receptors work?

A
  • they bind and pass through the cell membrane and enter the nucleus
  • as a dimer this binds to glucocorticoid response elements (GRE) in promoter sequence and activates transcription
  • as a monomer it represses transcription
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22
Q

what two receptors do glucocorticoids bind to?

A

GR and MR

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23
Q

what is the negative consequence of glucocorticoids binding to MR

A

triggers cutaneous adverse effects e.g. skin atrophy and delayed wound healing

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24
Q

three types of signalling

A
  1. autocrine
  2. paracrine
  3. endocrine
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25
Q

define autocrine signalling

A

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

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26
Q

define paracrine signalling

A

chemicals are released from cells bind to receptors on adjacent cells

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27
Q

define endocrine signalling

A

chemicals are transported via circulatory system to act on distant cells

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28
Q

two types of feedback control

A

negative

positive

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29
Q

two co-ordinated regulatory systems

A
  • intrinsic

- extrinsic

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30
Q

factors that cause homeostatic end points to vary

A 
genetics
age
gender
health status 
environment
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31
Q

actions of insulin

A
  • induces glucose uptake and utilisation by cells (muscles and liver)
  • promotes glycogenesis and lipogenesis
  • stimulates amino acid uptake and protein formation
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32
Q

define type 2 diabetes mellitus

A

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

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33
Q

aims of diabetes management

A

optimise blood glucose and decrease possible complications

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34
Q

non-pharmacological management of diabetes

A 
lifestyle changes 
smoking
diet
weight
exercise
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35
Q

two modes of action of pharmacological therapies

A
  1. dependent upon insulin

2. independent upon insulin

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36
Q

dependent upon insulin therapy action

A

increase secretion/ decrease resistance and hepatic glucose output

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37
Q

independent upon insulin mode of action

A

slowing absorption from the GI tract/ enhancing excretion by kidney

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38
Q

how is insulin secreted by the pancreatic beta cell?

A
  • elevation of blood glucose leads to increased facilitated diffusion through GLUT2 into the beta cell
  • glucose is phosphorylated by glucokinase
  • glycolysis of glucose-6-phosphate in mitochondria yields ATP
  • increased ATP closes ATP-sensitive K+ channels leading to membrane depolarisation
  • opens Ca2+ channels and increased intracellular Ca2+ triggers insulin release
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39
Q

define sulfonylureas (SUs)

A

insulin secretagogues

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40
Q

what do SUs require?

A

functional beta cells

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41
Q

what do SUs require?

A

functional beta cells, so efficacy can reduce with time

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42
Q

what do all agents in the SU class contain?

A

the sulfonylurea moiety (sulphur and oxygen)

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43
Q

action of SUs

A

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

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44
Q

what do SUs do?

A

decrease fating and post-prandial blood glucose and long-term microvascular complications

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45
Q

how are SUs administrated?

A

orally

peak release is 1-2 hours

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46
Q

short-acting SUs

A

tolbutamide

gliclazide

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47
Q

long-acting SUs

A

glibenclamide

glipizide

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48
Q

adverse of SUs

A

hypoglycaemia (increased risk in long-acting agents, elderly, reduced hepatic/renal function CKD)
undesirable weight gain (anabolic effect of insulin and appetite increased with urinary loss of glucose decreased)

49
Q

when are SUs used?

A

first line for those intolerant to metformin or with weight loss
second line in conjunction with metformin

50
Q

which drugs decrease the action of SUs?

A

thiazide diuretics

corticosteroids

51
Q

examples of glinides

A

repaglinide

nateglinide

52
Q

action of glinides

A

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

53
Q

how are glinides administered?

A

orally
rapid onset (30-60 minutes) and off set 4 hours
used in response to meals

54
Q

role of glinides

A

reduce post-prandial glucose

less likely to cause hypoglycaemia

55
Q

when are glinides used?

A

in conjunction with metformin and TZDs

56
Q

how is repaglinide metabolised?

A

hepatic metabolism and thus safer in CKD

57
Q

what is the incretin effect

A

insulins has a greater response to oral glucose than IV

58
Q

what happens with oral glucose?

A
  • ingestion 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
59
Q

two classes of drugs that work based on the incretin effect

A

DPP-4 inhibitors

Incretin analogues

60
Q

examples of DPP-4 inhibitors

A 
sitagliptin
saxagliptin
vildagliptin
linagliptin
alogliptin
61
Q

is the incretin effect reduced in T2DM?

A

yes

62
Q

how can the incretin effect be restored in T2DM

A

reducing breakdown of endogenous incretins

administering exogenous incretins resistant to breakdown

63
Q

what terminates the action of GLP-1 and GIP within minutes?

A

enzyme dipeptidyl peptidase- 4

64
Q

action of gliptins?

A

competitively inhibit DPP4, causing insulin secretion to be preserved

65
Q

when are gliptins used?

A

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

66
Q

adverse of DPP4-inhibitors (gliptins)

A

nausea
no hypoglycaemia
weight is neutral as they are weak drugs

67
Q

examples of incretin analogues

A

extenatide

liraglutide

68
Q

role of incretin analogues

A

mimic the action of GLP-1 but resist breakdown by DPP-4
agonists of GPCR GLP-1 receptors that increase intracellular cAMP concentration stimulating insulin release, also suppress glucagon, slow gastric emptying and decrease appetite

69
Q

positives of incretin analogues

A

weight loss

reduce hepatic fat accumulation

70
Q

how are incretin analogues administered?

A

SC weekly

71
Q

adverse of incretin analogues

A

nausea

rarely pancreatitis

72
Q

examples of alpha glucosidase inhibitors

A

acarbose
miglitol
voglibose

73
Q

describe alpha glucosidase

A

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

74
Q

when are alpha glucosidase inhibitors taken?

A

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

75
Q

adverse of alpha glucosidase inhibitors

A

flatulence
loose stools
diarrhoea (undigested carbohydrate and colonic bacteria)

76
Q

which drug is infrequently used in the UK?

A

alpha glucosidase inhibitors

77
Q

example of biguanides

A

metformin

78
Q

which drug is first line in T2DM?

A

metformin

79
Q

can metformin be used in kidney disease

A

no as it accumulates

80
Q

action of metformin (biguanide)

A

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

81
Q

desirable effects of metformin

A

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

82
Q

adverse of metformin (biguanide)

A

GI upset

rarely lactic acidosis (hepatic/renal disease and excess alcohol)

83
Q

role of thiazolidinediones (TZDs)

A

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

84
Q

what do TZDs act on?

A

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

85
Q

desirable effects of TZDs

A

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

86
Q

adverse of TZDs

A 
weight gain
fluid retention (promote Na+ reabsorption by the kidney)
87
Q

specific drugs in TZDs class

A

ciglitzone
troglitzone
pioglitzone

88
Q

what is the only TZD used and why?

A

pioglitzone as ciglitzone and troglitzone cause serious hepatotoxicity

89
Q

what can TZDs be used in combination with?

A

metformin or SUs

90
Q

what patients is TZDs used in?

A

obese people as it shifts fat from visceral and liver

91
Q

do SGLT2 inhibitors require insulin

A

no

92
Q

what does sodium-glucose cotransporter-2 inhibitors act on?

A

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

93
Q

benefits of SGLT2i

A

decrease blood glucose with little risk of hypoglycaemia

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

94
Q

agents in SGLT2i

A

dapaliflozin
canagliflozin
empagliflozin

95
Q

adverse of SGLT2i

A

increased risk of thrush

96
Q

what other diseases benefit in SGLT2i?

A

CVS

renal

97
Q

define insulins somogyi effect

A

taking insulin at night causes on waking very high blood glucose levels due to blood sugar being lowered too much

98
Q

what provides the highest level of endocrine control?

A

the hypothalamus

99
Q

how does the hypothalamus integrate endocrine and nervous system?

A
  • secretes regulatory hormones which control activity of anterior pituitary cells
  • synthesises hormones and transports them to the posterior pituitary via the infundibulum
  • hypothalamic autonomic control centres control secretion of adrenaline and NA by the adrenal medulla
100
Q

describe the diurnal (circadian rhythm) control of hormone levels

A
  • external cues (light/dark) evoke fluctuations in hormone secretions
  • hormone levels are influences by the rate at which they are eliminated from the body
101
Q

example of a female steroid hormone?

A

oestrogen

102
Q

what are steroid hormones made of?

A

lipids derived from cholesterol

103
Q

are steroid hormones stored?

A

no, once they are synthesised they are secreted

104
Q

how are steroid hormones transported?

A

hydrophobic and transported in the blood plasma by binding to carrier proteins

105
Q

when are steroid hormones biologically active?

A

when they are unbound
they pass through the membrane forming an activated hormone-receptor complex which binds to DNA and activates specific genes to produce specific proteins

106
Q

example of an amine hormones

A

adrenaline

107
Q

three classes of hormones

A

steroid
amine
peptide and protein

108
Q

describe how catecholamines are transported?

A

hydrophilic and transported unbound in blood plasma

109
Q

describe how thyroid amines are transported?

A

bound to carrier proteins

110
Q

two types of amine hormones

A

thyroid amines

catecholamines

111
Q

what are amine hormones made of?

A

amino acids

112
Q

are amine hormones stored?

A

yes in vesicles until needed and they bind to membrane bound receptors

113
Q

examples of peptide hormones

A

oxytocin

ADH

114
Q

examples of protein hormones

A

GH

insulin

115
Q

how are peptide and protein hormones transported?

A

they are hydrophilic and transported unbound in blood plasma

116
Q

how are protein and peptide hormones synthesised?

A

precursor molecules and stored in secretory vesicles and cleaved by enezymes

117
Q

what does the binding to carrier proteins facilitate?

A

hormone transport
increased half-life
reservoir of hormones

118
Q

specific carrier proteins

A

cortisol-binding globulin (CBG)
thyroxine-binding globulin (TBG)
sex steroid-binding globulin (SSBG)

Endocrine: Basic Science (7 decks)

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