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Year 2 - Endocrinology (DP) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What sort of glands are in the endocrine system?

A

Ductless

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2
Q

How is signal specificity achieved?

A

Chemically distinct hormones
Specific hormone receptors
Distinct receptor distribution

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3
Q

What are the features of amine hormones? (Synthesis, storage, release and transport)

A 
Pre-synthesised:
     - Formed by enzymes
Stored in vesicles
Released in response to calcium
Transported free in plasma (hydrophilic)
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4
Q

What are the features of peptide + protein hormones? (Synthesis, storage, release and transport)

A 
Pre-synthesised:
     - From longer precursor via proteolysis
Stored in vesicles
Calcium causes release
Transported free in plasma
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5
Q

What are the features of steroids hormones? (Synthesis, storage, release and transport)

A

Synthesised and secreted on demand
Stimuli increase:
- Cholesterol uptake
- Rate of conversion to pregnenolone (rate limiting)
Transport:
- 90% bound to plasma proteins (lipophilic)
- Free if biologically active

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6
Q

What hormones are insoluble?

A

Steroids

Thyroxine

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7
Q

What are the functions of carrier proteins?

A

Increase hormone transport in blood
Prevent renal filtration
Prevent rapid excretion

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8
Q

What does cortisol-binding globulin bind?

A

Cortisol

+ aldosterone

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9
Q

What does thyroxine-binding globulin bind?

A 
T4 selectively
(+ some T3)
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10
Q

What does SHBG bind?

A

Testosterone

Oestradiol

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11
Q

What do albumin and transthryretin bind?

A 
Albumin:
     - Steroids
     - T4
Transthyretin:
     - T4
     - Some steroids
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12
Q

What do carrier proteins act as?

A

Buffers and reservoirs:

 - Main constant [Free hormone] in blood
 - Keep bound and free hormones in equilibirum
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13
Q

What hormones can cross capillary walls?

A

Free hormones

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14
Q

What happens when free hormone is removed from the plasma?

A

Replaced by dissociation of bound protein

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15
Q

What is the primary determinant of hormone plasma concentration?

A

Rate of secretion

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16
Q

What does neuroendocrine release cause?

A

A sudden burst in secretion to meet a stimulus:

- eg. Stress -> Hypothalamus -> CRH -> ACTH -> Cortisol

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17
Q

How does diurnal rhythm release work?

A

Secretion fluctuates with time

Entrained to external cues (Night/Day)

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18
Q

What organs are the most important locations for elimination of hormones?

A

Liver

Kidney

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19
Q

What are the half lives of:

  • Amine hormones
  • Protein/Peptide hormones
  • Steroids/T3 +T4
A

Amines -> Seconds
Proteins/Peptides -> Minutes
Steroids/T3+T4 -> Hours to days

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20
Q

What affects the half lives of hormones?

A

Protein binding

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21
Q

Where are G-protein coupled receptors found and what hormones activate them?

A

On cell surface
Activated by:
- Amines
- Some proteins/peptides

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22
Q

What do G-protein coupled receptors couple with?

A

Gs
Gi
Gq

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23
Q

Where are receptor kinases found and what hormones activate them?

A

On cell surface

Activated by some proteins and peptides

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24
Q

Where are nuclear receptors found and why are they found here?

A

Intracellularly:
- Ligands are lipophilic
> Can diffuse across cell membrane

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25
What activates Class 1 Nuclear receptors? What happens when they are activated?
Many steroids: | - Migrate to nucleus on binding
26
What happens when Class 1 Nuclear Receptors are inactive?
Bound to inhibitory heat shock proteins in the cytoplasma
27
What activates Class 2 Nuclear receptors? Where are they found?
Mostly by lipids | In the nucelus
28
What activates the hybrid class nuclear receptors? What are they similar to?
T3 (+others) | Similar to Class 1
29
What happens when adrenaline, CRH or glucagon binds to a GPCR?
1. Gs subunit uncouples 2. Binds to adenylyl cyclase 3. Promotes ATP -> cAMP 4. cAMP activates Protein Kinase A 5. Target protein phosphorylation -> Effects
30
What happens when melatonin binds to a GPCR?
1. Gi subunit uncouples 2. Binds to adenylyl cyclase 3. Inhibits ATP -> cAMP 4. Less Protein Kinase A activation 5. Less target protein phosphorylation -> Inhibits effects
31
What happens when angiotensin ii, GRH or TRH binds to a GPCR?
1. Gq subunit uncouples 2. Binds to phospholipase C 3. Promotes PIP2 -> IP3 4. IP3 binds to IP3 receptor on endoplasmic reticulum 5. Calcium released 6. Cellular effects
32
What other effects does the hydrolysis of PIP2 to IP3 have?
1. Produces DAG 2. DAG activates Protein Kinase C (in membrane) 3. Target proteins are phosphorylated -> Effects
33
What happens when insulin binds to a receptor kinase?
1. Autophosphorylation of intracellular tryosine residues 2. Insulin receptor substrate proteins are phosphorylated 3. Cellular effects
34
How does signalling via Class 1 Nuclear Receptors work?
1. Steroid diffuses into cell 2. Binds to intracellular receptor + HSP dissociates 3. Moves to nucleus 4. Forms a dimer + binds to hormone response elements in DNA 5. Transactivation or Transrepression occurs 6. mRNA levels altered 7. Rate of protein synthesis changes 8. Protein levels altered
35
What drugs increase insulin secretion?
SUs Incretin mimetics Glinides DPP-4 inhibitors (Gliptins)
36
What drugs reduce insulin resistance and reduce hepatic glucose output?
Biguanides | TZDs (Glitazones)
37
What drugs slow glucose absorption from the GI tract?
α-glucosidase inhibitors
38
What drugs increase glucose excretion in the kidneys?
SGLT2 inhibitors
39
Which drugs are insulin dependent and which are insulin independent?
``` Insulin-dependent: - SUs - Incretin mimetics - Glinides - DPP-4 inhibitors - Biguanides - TZDs Insulin-independent: - α-glucosidase inhibitors - SGLT2 inhibitors ```
40
What is the physiology of insulin secretion?
1. Increased blood glucose 2. Increased glutamate diffusion into B-cell via GLUT2 3. Phosphorylation of glucose by glucokinase 4. Glycolysis of glucose-6-phosphate in mitochondria 5. Increased ATP/ADP ratio 6. ATP sensitive K+ channels close 7. Depolarisation 8. Voltage-gated calcium channels open 9. Increased intracellular [Calcium] 10. Insulin secretion
41
What is the structure of the Katp channel?
4 inward K+ rectifier 6.2 subunits (Kir6.2) | 4 sulphonylurea receptor 1 subunits (SUR1)
42
What is the function of the Kir6.2 tetramer?
Selective K+ channel
43
What is the function of the SUR1 tetramer?
Regulates K+ channel activity
44
When does ATP bind to Kir6.2?
When [Glucose]e is high
45
When does ADP-Mg2+ bind to SUR1?
When [Glucose]e is low
46
What are some examples of SUs?
1st generation - Tolbutamide 2nd generation: - Glibenclamide - Glipizide
47
How do SUs work?
Displace ADP-Mg2+ from SUR1: | - Closes channel
48
What benefits do the 2nd generation SUs have over 1st generation?
More potent | Longer-acting
49
Who are at the greatest risk of hypos with SU use?
People using 2nd generation SUs Elderly people Patients with reduced hepatic/renal function
50
What can SUs be used with?
Metformin | TZDs
51
What effect do SUs have on weight?
They cause weight gain
52
How do glinides/meglitinides work?
Bind to SUR1 at benzamido site (close channel -> depolarization -> Insulin release)
53
What are some examples of glinides?
Repaglinide | Nateglinide
54
When are glinides taken? Why?
Before meals: | - Reduce post-prandial rise in blood glucose
55
What can glinides be used with?
Metformin | TZDs
56
When are GLP-1 and GIP released? From what cells are they released?
When food is ingested Released from: - L cells - K cells
57
Where do GLP-1 and GIP enter?
Portal blood
58
What effects does GLP-1 have?
Increase insulin release from β-cells | Decrease gastric emptying
59
What effects does GIP have?
Reduce glucagon release from α-cells
60
Whet are the downstream effects of GLP-1 and GIP?
Enhanced glucose uptake + utilisation | Reduced glucose production
61
How do incretin analogues work?
Mimic GLP-1 action but are longer lasting
62
What is exenatide?
Synthetic extendin-4: - A GLP-1 agonist - Peptide in saliva of Gila monster
63
How does exenatide work?
Binds to GPCR GLP-1 receptors -> Increased [cAMP]i: - Increased insulin secretion - Reduced glucagon secretion - Reduced gastric emptying - Reduced appetite
64
What other effects do incretin mimetics have?
Modest weight loss | Reduced hepatic fat accumulation
65
How is exenatide administered?
S/C injection twice daily
66
How is liraglutide administered?
S/C injection once daily
67
What side effects can incretin mimetics have?
Nausea Hypos Pancreatitis (rare)
68
What does dipeptidyl peptidase-4 do?
Terminates GLP-1 and GIP action (in minutes)
69
What do DPP-4 inhibitors (gliptins) do?
Competitively inhibit DPP-4: | - Prolong GIP and GLP-1 actions
70
What are DPP-4 inhibitors usually used with?
TZDs | Metformin
71
What are some examples of DPP-4 inhibitors?
Sitagliptin Saxigliptin Vildagliptin
72
How often must DPP-4 inhibitors be administered?
Once daily PO
73
If used as monotherapy, can DPP-4 inhibitors cause hypos?
No
74
What effect do DPP-4 inhibitors have on weight?
They are weight neutral
75
What is α-glucosidase? What does it do?
A brush border enzyme: | - Starch and disaccharides -> Glucose
76
What does acarbose to?
Inhibits α-glucosidase and delays glucose absorption: | - Reduces post-prandial rise in blood glucose
77
When is acarbose used?
In T2DM is other drugs don't work
78
What are some side effects of acarbose?
``` Flatulence Loose stools Diarrhoea Abdominal pain Bloating ```
79
Does acarbose have any risk of hypos?
No
80
What is the only therapeutic biguanide?
Metformin
81
When is metformin the 1st line for T2DM?
In obese patients: | - With normal hepatic + renal function
82
What other effects does metformin have?
Reduces hepatic gluconeogenesis -> Stimulates AMPK Increased glucose uptake and utilisation Reduces carbohydrate absorption Increased fatty acid oxidation
83
What effect does metformin have on weight?
Reduces it
84
What can metformin be combined with?
SUs TZDs Insulin
85
What are some side effects of metformin?
``` GI upset: - Diarrhoea - Nausea - Anorexia Lactic acidosis -> Avoid in hepatic/renal impairment ```
86
What do thiazolidinediones (glitazones) do?
Enhance action of insulin at target sites
87
How do TZDs work?
Exogenous agonists of peroxyisome proliferator-activated receptor-γ (PPARγ): - Associated with retinoid receptor X (RXR) - Largely confined to adipocytes
88
What does activated PPARγ-RXR act as?
``` Transcription factor: - Binds to DNA - Increases gene expression - Increased protein encoding > Insulin signalling > Lipoprotein lipase, FFA transport + GLUT4 ```
89
What are some desirable effects of TZDs?
Fatty acid uptake and storage in adipocytes | Reduce hepatic glucose output
90
What are some adverse effects of TZDs?
Increased weight due to adipocyte differentiation Fluid retention due to increased Na+ reabsorption Hepatotoxicity: - Ciglitazone - Troglitazone Increased bone fractures
91
What TZD can be used with metformin and SUs?
Pioglitazone
92
How do SGLT2 inhibitors work?
Block reabsorption of glucose in PCT: | - Causes deliberate glycosuria
93
What effect do SGLT2 inhibitors have on weight?
Weight loss: - Calorific loss -> Glucose voided - Water loss -> Osmotic diuresis
94
What is the only licensed SGLT2 inhibitor?
Dapaglifozin

Year 2 - Endocrinology (DP) (15 decks)

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