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BMS2021 > TOPIC C: Autonomic control of energy and metabolism > Flashcards

TOPIC C: Autonomic control of energy and metabolism Flashcards

1
Q

Which type of receptors do NA and A target?

A
  • GPCR (G protein coupled receptors)
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2
Q

What is the main role of NA in context of metabolism and energy?

A
  • Provide energy, alertness, concentration (focus)
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3
Q

Is NA a neurotransmitter or hormone?

A
  • Neurotransmitter
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4
Q

Is A a neurotransmitter or hormone?

A
  • Hormone
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5
Q

What does the speed of the response depend on in cells?

A
  • The receptor type (class)
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6
Q

What do receptors respond to?

A
  • Endogenous substances in boy (activated receptors)
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7
Q

What two roles can drugs have on receptors?

A
  1. ADD to level of receptor activation (enhanced level of activation)
  2. PREVENT receptor activation (repressed level of receptor activation)
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8
Q

What is the main NT for the sympathetic ns?

A
  • NA
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9
Q

Which two types of receptors can be affected with NA?-

A
  • Alpha adrenoceptros

- Beta adrenoceptors

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10
Q

How is NA synthesied and where?

A
  • Synthesised in nerve endings

- enzymes are transported down TO nerve endings

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11
Q

Does NA have to be stored in vesicles?

A
  • YES! Otherwise it will break down.
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12
Q

What are the steps of NA synthesis?

A
  • Tyrosine enters nerve ending via PRECURSOR TRANSPORTER
  • Tyrosine —-> DOPA via TYROSINE HYDROXYLASE
  • DOPA— Dopamine via DOPA DECARBOXYLASE
  • Dopamine transported into synaptic storage vesicle via VMAT (Vesicular Monoamine transport)
  • Dopamine–> NA via DOPAMINE BETA HYDROXYLASE
  • Action potential opens Ca2+ channels to allow synaptic vesicles to move to nerve terminal and NA is exported.
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13
Q

Which two ways is NA terminated (Action)?

A
  1. REUPTAKE into nerves (MOST IMPORTANT FACTOR) -Like to reuse NA
  2. Enzymatic breakdown (via MAO)–> MAO found in mito.
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14
Q

Which well known drug blocks reuptake of NA?

A
  • Cocaine (increased and prolonged effects of SNS)
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15
Q

Where is Adrenaline synthesised and released into?

A
  • Synthesized in the adrenal medulla and released into bloodstream where it is circulating hormone
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16
Q

What is the precursor for adrenaline and enzyme that converts it?

A
  • NA is precursor for A

- PNMT is enzyme that converts NA–> A in adrenal medulla

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17
Q

Which adrenoceptor increases force and HR, Slows/relaxes gut activityand relaxes/dilates smooth muscle to INCREASE BLOOD FLOW?

A

-BETA adrenergic receptors

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18
Q

Why can our tissues have different effects despite the same beta adenoceptors?

A

-It depends on the type of enzymes that are coupled to G protein receptor -different enzymes coupling to receptor will cause different effects

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19
Q

For beta receptors, which protein is phosphorylated and what is the response in the LIVER?

A
  • Glyogen phosphorylase is protein (enzyme) —> glycogenolysis—-> increased glucose—> energy (glycolysis)
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20
Q

For beta receptors, which protein is phosphorylated and what is the response in the CARDIAC MUSCLE (HEART)?

A
  • Troponin/phosphoholamban is protein

- Leads to INCREASED HR and INCREASED force of contraction

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21
Q

For beta receptors, which protein is phosphorylated and what is the response in the SMOOTH MUSCLE?

A
  • Myosin light chain is protein

- Leads to relaxation

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22
Q

Are there multiple Beta receptors?

A
  • YES!
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23
Q

Where are Beta1 receptors found?

A
  • In cardiac muscle (increased force of contraction and HR)
  • Liver
  • Skeletal muscle (blood vessels)
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24
Q

Where are Beta 2 receptors found?

A
  • Lungs (bronchiole smooth muscle)
  • Blood vessel beds in skeletal muscle
  • Leads to relaxation
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25
Q

Where are Beta 3 receptors found?

A
  • Fat (adipose)
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26
Q

What are 4 things the sympathetic nervous system does in exercsie?

A
  1. Liver releases glucose
  2. Heart pumps faster
  3. Breathing fast
  4. Oxygen needed for muscles
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27
Q

In exercise; i. what effect, ii: which receptor iii. Does an increase or decrease result from beta adrenoreceptors in:
LIVER?

A

i. Glycogenolysis effect
ii. Via Beta 1 receptor
iii. Leads to an INCREASE in activity of adrenoceptors

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28
Q

In exercise; i. what effect, ii: which receptor iii. Does an increase or decrease result from beta adrenoreceptors in:
SKELETAL MUSCLE?

A

i. Glycogenolysis effect via Beta 1
Glucose uptake via beta2
thermogenesis via beta 3
- acts to INCREASE activity

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29
Q

In exercise; i. what effect, ii: which receptor iii. Does an increase or decrease result from beta adrenoreceptors in:
WAT (white adipose tissue)?

A
  • Lipolysis effect
  • Via beta 3 receptors
  • Acts to INCREASE response
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30
Q

What does BAT do (Brown Adipose tissue)?

A
  • Thermogenesis (non shivering)

- Via B3 receptors to increase activity

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31
Q

What do Adrenaline and NA encourage (metabolism terms)

A
  • Encourages glycogen and fat to form glucose and FAs–> GNG–> energy
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32
Q

What is the Beta `1 receptors effect on metabolism? (which tissues is it in and what does it cause)

A
  • LIVER-> stimulates glycogenolysis
  • Glycogen phosphorylase ACTIVATED and glycogen synthase INHIBITED
  • SKELETAL MUSCLE: Stimulates glycogenolysis
  • Stimulates glucose uptake into muscle cells INCDEPENDENT of insulin
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33
Q

Do adrenoceptors affect BOTH brown and white adipose tissue?

A
  • YES
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34
Q

What are WATs mainly used for?

A
  • Energy storage
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35
Q

What are BATs mainly used for?

A
  • Specialised for heat production
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36
Q

Are FAs from WAT or BAT released during fasting?

A
  • WAT
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37
Q

What are the characteristics of WAT?

A
  • Single large lipid droplet
  • FEW mitochondria
  • Excess energy stored as triglycerides
  • FAs released during fasting
  • Activated by circulating adrenaline
  • Innervation..not sure
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38
Q

What are the characteristics of BAT?

A
  • MULTIPLE small lipid droplets
  • LOTS of mitochondria
  • Densly vascularised
  • Innnervated by sympathetic nerves
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39
Q

Where is white fat found?

A
  • Where fat people have it
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40
Q

Where is brown fat found?

A
  • Suprarenal
  • Paravertebral
  • Paraaortic
  • Supraclavicular
41
Q

What activates brown adipose tissue?

A
  • Cold temperature
42
Q

Typically, does a lean person have more BAT activated than white compared to a fat person?

A
  • YES
43
Q

What allows for heat generation in brown fat?

A
  • Mitochondria have UCP-1 (uncoupling protein 1)
44
Q

What is the pathway for Beta3 adrenoceptor activation in BAT?

A
  • Final activation of lipase
  • GPCR/Beta3 activation of adenylate cyclase –> cAMP–> PKA + Phosphorylation and activation of lipase –> triglycerides –> free FAs
45
Q

Which process produces long chain FAs which then upregulate the expression of UCP-1 (in oxidative phosphorylation)?

A
  • The Beta oxidation process
46
Q

What are possible treatments for obesity based on BAT and Beta 3 adrenoceptors?

A
  • Cold stimulation + NA= best inducer of brown fat

- Possible use of Beta3 agonist in obesity –> increases lipolysis and energy expenditure

47
Q

Can beta3 agonist secretion turn white fat cells into brown fat cells?

A
  • YES! (sort of more of a beige fat adipose tissue –> produces heat)
48
Q

What does a Beta1 adrenoceptor antagonist do (betablocker)?

A
  • REDUCES exercise tolerance (not a lot of increased blood flow vessels)
  • LOWERS BP and CO (Only affects the active state, not if you are resting)
49
Q

Is bronchiole smooth muscle innervated by the sympathetic nervous system?

A
  • NONONO!!!

- Beta2 receptors in lungs rely on circulating ADRENALINE (hormone) to activate them

50
Q

What effect do Beta2 receptors have when stimulated in the lungs?

A
  • In the lungs ) they cause BRONCHODILATION /mediate it
51
Q

What type of drug would you give to someone with an asthma attack?

A
  • Beta 2 agonist (to dilate the airways)
52
Q

What will the Beta2 antagonist do in asthmatics?

A
  • Brocnhospasm (worsening of airway) `
53
Q

Are there Beta2 receptors in muscle (like actual muscle, not blood vessels in muscle) ?

A
  • YES!!
  • A or NA affects the speed of twitchign of different faet twitch or slow twitch fibres –> leads to muscle tremor
  • Increases the amount of fast twitch fibres.
  • Beta2 receptor agonist
    e. g. Salbutamol (asthma drug) -> muscle tremor as side effect
54
Q

What is the effect of beta blockers (beta2 antagonists) in the skeletal muscle?

A
  • Removes the muscle tremor (nervousness) –> sympathetic response
55
Q

What is the effect of a beta2 agonist in skeletal muscle?

A
  • INCREASES the twitch tension of fast muscle fibres and DECREASES the tension of slow twitch muscle fibres
  • INCREASES the INSTABILITY of reflex control of muscle length (temor)
56
Q

What are 4 general effects of a beta adrenoreceptor antagonist?

A
  • Steadiness of voluntary muscle
  • Fatigue (blocking of B1 receptors in heart)
  • Cold extremities (blocking Beta2 vasodilator in blood vessels
  • Narrowing of bronchi (poor exercise tolerance)
57
Q

What are 5 general effects of a Beta adrenoreceptor agonist?

A
  • INCREASE in HR and FORCE –> increase in exercise capacity
  • Activation of Beta1 receptors in heart –> increase in cardiac function/capacity
  • INCREASE in blood flow to voluntary muscles –> activation of vasodilator beta2 receptors on BLOOD VESSELS
  • Widening of bronchi–> increases exercise tolerance and O2 delivery (b2 on lung)
  • Increases muscle tremor
58
Q

What type of drug is clenbuterol?

A
  • Beta2 receptor agonist
  • Bronchodilator
  • Increases oxygen uptake
  • Skeletal muscle fast and slow twitch
59
Q

What is pharmacokinetics and which 4 factors does pharmacokinetics include?

A 
How body INTERACTS with drug 
Absorption
Distribution 
Metabolism
Excretion 
= ADME
60
Q

What is pharmacodynamics and which 3 factors does this include?

A

Binding to target tissue (receptor)
Efficacy (ability of drug to get its job done well)
Affinity

61
Q

Do drugs have to have a good balance of lipid and water solubility?

A
  • YES!

- Because most of body is WATER BUT also has to get into cells

62
Q

What do drugs have to get into in order to rapidly spread around body?

A

into SYSTEMATIC CIRCUIT

63
Q

What are the 4 main routes of administration of drugs?

A
  • Injections
  • Sublingual
  • Rectal
  • Oral
64
Q

What are the details of injections for drug routes?

A
  • goes into the SYSTEMIC circuit

- have a RAPID onset , especially IV

65
Q

What are the details of a drug given sublingually and where does it go directly to, also why is this type of administration good (what does it avoid) ?

A
  • goes directly to VENA CAVA
  • Good because it avoids the stomach acids which contains enzymes that can break drug down
    e. g drug: Nitroglycerin
66
Q

What is the pathway for the oral route of drug administration?

A
  • needs to go through stomach/small intestine (absorbed)–> then into SYSTEMIC CIRCULATION (takes longer)
67
Q

Where are the final targets for drugs?

A
  • SYSTEMIC CIRCULATION and plasma (levels in plasma depend)

- Needs to access all body organs/cells (mostly)

68
Q

To gain access to all organs and most cells what must the drug be like?

A
  • Must be LIPID SOLUBLE to pass through all cell layers BUT must have some H2O property to be in the SYSTEMIC CIRCULATION
69
Q

Where will drugs remain if they are inhaled?

A
  • Only in the lungs
70
Q

What is a key property that drugs must have to leave the body?

A
  • Water soluble (hydrophillic)
71
Q

What does the liver do to metabolites in terms of excreting them?

A
  • Makes metabolites that are more water soluble for EXCRETION
72
Q

Do drugs move across ALL body compartments?

A
  • YES! Must be in equilibrium…e..g if drug is removed from plasma drug will come out of cell to equalize
73
Q

What happens when you are put under a general anaesthetic?

A
  • Have to get injection first –> thiopentone (induction anaethetic SHORT ACTING barbituate (10-20 secs) -has fast access to brain –> unconsciousness
  • then a tube is put into trachea and GAS put in that maintains the unconsciousness
74
Q

Why does thiopentone have fast access to the brain and only lasts for a short amount of time?

A
  • Because it is LIPID SOLUBLE

- Will quickly leave bloood –> BRAIN –> muslce –> fat

75
Q

IF a drug is already water soluble, does it get metabolsied as much?

A
  • NO

- just excreted –> unchanged

76
Q

Where are the products formed to be more lipid soluble?-

A
  • In LIVER –> byproducts –> biotransformed –> excreted in urine
77
Q

Can liver break down drug into toxic metabolites?

A
  • YES

- This is why drugs need to be tested

78
Q

What does metabolism in the liver occur via?

A
  • Liver microsomal enzymes (also happens in gut and kidney)
79
Q

Are all drugs active when entering body?

A

NO! Some are pro-drugs

- Must be activated by metabolism

80
Q

How are drugs excreted?

A
  • Filtered by KIDNEY (urine)

- Faesces, bile ,lungs(expelled air)

81
Q

Which 3 ways can drugs be metabolised and excreted in liver?

A
  1. Drug–> Phase I–> Phase II–> Excretion
  2. Drug—————-> Phase II–> Excretion
  3. Drug ——————————-> Excretion (no change, very polar drug)
82
Q

What occurs in phase I of liver metabolism of drug and which class of enzymes is contained here?

A

Oxidation
Reduction
Hydrolysis
- All act to produce a more water soluble metabolite
- Contain CYTOCHROME P450 ENZYMES (liver microsomal enzymes)

83
Q

What occurs in phase II of liver metabolism of drug?

A
  • Metabolite combined with endogenous molecule e.g. glucuronide acetyl –> produces an EVEN MORE water soluble molecule
  • Contains UDP glycuronysl transferase enzyme
84
Q

What is the role of cytochrome p-450 (CYP) enzymes?

A
  • Can degrade endogenous substances and has role in biosynthesis (steroids lipids vitamins)
  • Metabolises xenobiotics
85
Q

Are there lots of different P-450 family enzymes?

A
  • YES!
86
Q

Which families are most of the metabolising drug enzymes found in?

A
  • CYP 1, 2, 3 gene families
87
Q

What is the substrate specificity like for the CYP 1, 2,3 families?

A
  • BROAD substrate specificity (2 or more enzymes can catalyse the same reaction)
88
Q

What does he CYP3A4 enzyme belong to and where is it?

A
  • Belongs to family 3, subtype A,4

- In GI tract –> poor oral availability of drugs

89
Q

Which 6 factors can change the level and activity of Cyp enzymes?

A
  1. Nutrition
  2. Smoking
  3. Alcohol
  4. DRUGS
  5. Environment
  6. Genetic poylmorphisms (e.g. African)
90
Q

How come you shouldn’t eat grapefruit with some drugs such as statins?

A
  • Grapefruit can block enzyme action in small intestine
  • Grapefruit is an INHIBITOR of the enzyme that destroys the drug
  • INCREASES amount of medicine absorbed in body and thus a risk of overdose
  • BOTH DRUG + GRAPEFRUIT COMPETE AND INTERACT WITH CYP450 ENZYME
91
Q

What do enzyme inducers cause?

A
  • Enzyme inducers cause the drug to be matabolized quickly and fall below the normal range
92
Q

Which CYP enzyme do chargrilled food induce?-

A

CYP1A enzyme

93
Q

Which enzyme does grapefruit juice inhibit?

A
  • CYP3A
94
Q

Which enzyme in general does liver diseases such as cirrhosis, cancer, hemochromatosis, fatty liver inhibit?

A
  • P450 activity impaired

- Cardiac disease slows blood flow to liver which decreases metabolism

95
Q

Can metabolism of drugs lead to toxic metabolites?

A
  • YES e.g. paracetamol
96
Q

What toxic intermediate can paracetamol metabolism lead to if too much is ingested?

A
  • NAPQ1 (n-acetyl-p-benzoquinoneimine)

- Normally in low levels then CONJUGATED for excretion

97
Q

How is NAPQ1 normally detoxified?

A
  • By reacting with glutathione
98
Q

Which two ways can lead to paracetamol toxicity?

A
  • Glutathione is DEPLETED OR normal conjugation is prevented (too much panadol)
99
Q

Effects of NO GLUTATHIONE (paracetamol toxicity)`

A
  • NAPQ1 reacts with tiol groups on liver cell membrane –> hepatotoxicity–> Liver failure (35% liver failure from paracetamol poisoning)

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