Respiratory Disease Flashcards

1
Q

In which parts of the autonomic nervous system is ACh found?

A

pre-ganglionic neurons, post ganglionic parasympathetic + post-ganglionic sympathetic in sweating
released from motor neurons at the NMJ

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2
Q

In Ach an agonist or antagonist?

A

agonist (affinity + efficacy)

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3
Q

What type of receptor does it activate?

A

Nicotinic

Muscarinic

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4
Q

What are the effects of ACh transient?

A

broken down by cholinesterases eg. acetylcholinesterases + butrylcholinesterases

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5
Q

The action of ACh in the respiratory tract mimics the stimulation of which nerve?

A

vagus

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6
Q

What is airway resistance + what factors contribute to airway resistance in man?

A

AR = obstruction to airflow
The diameter of the lumen of the bronchioles decreases due to:
- physical means –> cartilage + interseptum junctions of alveoli
- ANS

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7
Q

How many histamine receptor types are there?

A

4

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8
Q

Where are they located?

A
H1 = smooth muscle, endothelium + CNS
H2 = parietal cells + vascular smooth muscle cells
H3 = CNS (+ peripheral NS to lesser extent)
H4 = basophils, bone marrow, thymus SI, spleen, colon
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9
Q

What does the H1 receptor do?

A
bronchoconstriction
bronchial smooth muscle contraction
vasodilation
endothelial separation --> HIVES
pain + itching die to insect stings
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10
Q

What physiological and pathophysiological states are the H1 receptors involved in?

A

allergic rhinitis
motion sickness
sleep
appetite suppression

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11
Q

What does the H2 receptor do?

A

vasodilation

gastric acid secretion

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12
Q

What does the H3 receptor do?

A

decreased neurotransmitter release

histamine, acetylcholine, noradrenaline, seretonin

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13
Q

What do H4 receptors do?

A

chemotaxis

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14
Q

What effect would administration of ACh or autonomic nerve stimulation of airway smooth muscle have on airway resistance? Outline what the graph of this would look like.

A

Airway resistance would increase

Log curve –> sigmoid shaped

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15
Q

How would adding a muscarinic antagonist affect the shape of this graph + why?

A

atropine –> competitive –> high dose of agonist to overcome its effects –> graph shifts RIGHT

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16
Q

What side effects would you expect muscarinic antagonists to have?

A
pupil dilation + blurred vision
loss of pupillary reflex
tachycardia
inhibition of secretions
anti-emetic effects
17
Q

How can you overcome the problems associated with muscarinic antagonists to produce a therapeutically useful drug?

A

give it locally

modify structure to make it more ionic –> more difficult for it to be absorbed

18
Q

Ipratropium bromide is a muscarinic antagonist currently used in the treatment of?

A

COPD + asthma

19
Q

What type of cell produces histamine in man?

A

mast cells

20
Q

Why are histamine antagonists not used for the day-to-day control of asthma?

A

as histamine is just one of many factors that can constrict the airways

21
Q

What precursor is involved in the production of leukotrienes?

A

arachidonic acid

22
Q

Which leukotrienes are produced in the airways? How do they affect airway resistance?

A

LTC4/D4/E4

bronchoconstrictors –> increase airway resistance

23
Q

What strategies can be used in asthmatics to reduce the effects of endogenous leukotrienes?

A

leukotriene antagonists

drugs that target leukotriene synthesis eg. 5-lipoxygenase blockers

24
Q

What endogenous compound normally activates beta-2 adrenoreceptors in the airway smooth muscle?

A

adrenaline

25
Q

What are the side effects of using adrenaline to treat bronchospasm?

A

dysrhythmias
severe hypertension
ventricular fibrillation

26
Q

What types of drugs are isoprenaline and salbutamol?

A
isoprenaline = non-selective beta adrenoceptor agonist
salbutamol = selective beta 2 adrenoceptor agonist
27
Q

What is the advantage of salbutamol over isoprenaline?

A

has no beta 1 effects eg. decreasing myocardial oxygen supply

28
Q

What signal transduction system is linked to the beta-2 adrenoceptor?

A

cAMP mediated effect –> Gs protein

29
Q

Outline the pathway which results in smooth muscle relaxation.

A

b2 adrenoceptor –> adenylyl cyclase –> converts ATP to cAMP –> activates cAMP dependent protein kinases
MLCK phosphorylates previous kinase which inactivates it

30
Q

Other than receptor activation, what is one way in which smooth muscle relaxation can be enhanced?

A

increase cAMP:
phosphodiesterase breaks down cAMP –> AMP
blocking this increases cAMP –> increases smooth muscle relaxation

31
Q

Why is aminophylline not routinely used to treat asthma?

A

many side effects