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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
what are the different types of hormone receptors
- G-protein coupled receptors - Receptor kinases - Nuclear receptors
26
what are the classes of nuclear receptors
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.
27
how signalling via receptor kinases works, using insulin as an example
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
28
signalling bia nuclear receptors class 1
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
29
what is the only biguanide used in diabetes
Metformin
30
what is the function of Metformin
Insulin sensitiser
31
usual starting dose for metformin
500mg twice a day
32
overall effects of Metformin
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
What are the additional effects of Metformin
``` Reduces triglycerides and LDL - improves lipid profiles Safe in pregnancy - Gestational DM - Pre-existing T2DM Polycystic ovarian syndrome (PCOS) NAFLD ```
34
Metformin side effects
GI side effects: Anorexia, nausea, vomiting, diarrhoea, abdo pain, taste disturbance Lactic Acidosis Liver failure Rash
35
MOI of Metformin
Reduces hepatic gluoconeogenesis [by stimulating AMP-activated protein kinase (AMPK)] Increases glucose uptake and utilization by skeletal muscle (increases insulin signalling)
36
what are sulphonylureas, give 2 examples
Insulin Secretagogues - Glicazide - Glipizide
37
SU's effects
Hyperglycaemia management: Reduces HbA1c by 15-20 mmol/mol by increasing insulin secretion Prevention of Microvascular complications
38
SUs side effects
Hypoglycamia Weight gain GI upset - headache Avoid in severe renal or hepatic failure
39
MOI of SU
- Displacing the binding of ADP-Mg2+ from the SUR1 subunit | - Thus closing the KATP channel and stimulating insulin release
40
what is Thiazolidinediones (TZD) and what is the only agent available
PPARgamma agonists | - Pioglitazone
41
TZDs effects
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
Function of TZDs
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
MOI of TZDs
- 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
what are the proteins involved in insulin signalling
Lipoprotein lipase Fatty acid transport protein GLUT4
45
Side effects of TZDs
Weight gain | Fluid retention
46
what are incretins
Intestinal Secretion of Insulin
47
examples of incretins
GIP from K cells GLP-1 from L cells (cells in the small intestines)
48
what do GLP-1 and GIP do
enhance (increment) insulin release from pancreatic β-cells (and delay gastric emptying)
49
what does GLP-1 do also
decreases glucagon release from pancreatic α-cells
50
what do these actions by GLP-1 and GIP lead to
enhanced glucose uptake and utlization + decreased glucose production = decreased blood glucose
51
what is Exenatide and what dose is given
GLP-1 Receptor Agonists | subcutaneously twice daily
52
MOI of Exenatide
- Binds to GPCR GLP-1 receptors that increase intracellular cAMP concentration - Increases insulin secretion, suppresses glucagon secretion, slows gastric emptying, decreases appetite
53
Effects of Exenatide
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
Side effects of Exenatide
Nausea | Pancreatitis
55
what GLP-1 Agonist can be given once daily
Liraglutide
56
how is the actions of GLP-1 and GIP terminated
rapidly by the enzyme DPP-4
57
what are Gliptins and what is there function
DPP-4 inhibitors | prolong the actin of GLP-1 and GIP
58
what are the benefits of DPP-4 inhibitors
Promote insulin secretion from pancreas without hypoglycaemia Suppress glucagon (which is increased in T2DM) Weight neutral
59
example of DPP-4 inhibitors
Sitagliptin
60
why are SGLT2 inhibitors different from other treatments
do not rely on insulin
61
MOI of SGLT2 inhibitors
selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney nephron to deliberately cause glucosuria
62
how does SGLT2 inhibitors get rid of the glucose
pee out the glucose | decrease uptake of sugar by roughly 1/4
63
positive affects of SGLT2 inhibitors
decrease in blood glucose with little risk of hypoglycaemia weight loss- Calorific loss and water accompanying glucose
64
side effects of SGLT2 inhibitors
sugar in urine | - increase in thrush and UTIs
65
example of SGLT 2 inhibitor
dapagliflozin
66
how is the Katp channel opened and closed
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
how do SUs work
bind to SUR1 and close the Katp channel causing depolarisation and insulin release
68
what are the parts of the Katp channel
Kir6.2 | SUR1
69
what are Glinides
Act similarly to the sulfonylureas – bind to SUR1 (at a distinct benzamido site) to close the KATP channel and trigger insulin release
70
examples of Glinides
repaglinide | nateglinide
71
why are Glinides used sometimes over SUs
Have rapid onset/offset kinetics – less likely to cause hypoglycaemia than sulfonylureas
72
what is alpha-glucosidase
brush border enzyme that breaks down starch and disaccharides to absorbable glucose
73
what do Inhibitors of α-glucosidase do
delay absorption of glucose thus reducing postprandial increase in blood glucose
74
when are Inhibitors of α-glucosidase used
in 2TDM patients inadequately controlled by life style measures or other drugs
75
what is an example of Inhibitors of α-glucosidase
Acarbose
76
side effects of Inhibitors of α-glucosidase
GI upset - loose stools, diarrhoea, abdominal pain, bloating
77
why are Inhibitors of α-glucosidase useful
pose no risk of hypoglycaemia

Endocrine SB (15 decks)

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