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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where are the parasympathetic ganglions found?

A

The cell bodies of pregalglionic fibres are located in the brainstem and the cell bodies of the postganglionic fibres are embedded in the walls of the bronchi and bronchioles

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2
Q

What does stimulation of postganglionic cholinergic fibres cause?

A

Bronchial smooth muscle contraction which is mediated by M3 musarinic ACh receptors on airway smooth muscle cells
Mucus secretion increases which is also mediated by M3 muscarinic ACh receptors on goblet cells

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3
Q

What does stimulation of postganglionic noncholinergic fibres cause?

A

Bronchial smooth muscle relaxation which is mediated by nitric oxide and vasoactive intestinal peptide (VIP)

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4
Q

What is the effect of the sympathetic division on

smooth muscle in airways?

A

Nothing - there is no innervation of bronchial smooth muscle in humans, but post-ganglionic fibres supply submucosal glands and smooth muscle of blood vessels

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5
Q

What does stimulation of the sympathetic division have on the rest of the airways?

A

Bronchial smooth relaxation via beta2-adrenoceptors on airway smooth muslce cells activated by adrenaline released from the adrenal glands
Decreased mucus secretion mediated by beta2-adrenoceptors on goblet cells
Increased mucociliary clearance by beta2-adrenoceptos on epithelial cells
Vascular smooth muscle contraction mediated by alpha1-adrenoceptors on vascular smooth muscle cells

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6
Q

What are the general mechanisms for excitation contraction coupling in smooth muscle cells

A

Transmitter or hormone activated a GPCR such as M3 which initiates a Gq/11 pathway that results in the influx of calcium from the sarcoplasmic reticulum to the cytoplasm via the IP3 receptor
Depolarisation can also activate a calcium channel which results in the activation of ryanodine which results in the influx of calcium from the cytoplasmic reticulum to the cytoplasm

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7
Q

How is contraction initiated in smooth muscle cells?

A

Calcium activates calmodulin which then activated MLCK (myosin light chain kinase) which then phophorylates the myosin cross bridge to allow for muscle contraction

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8
Q

Simply, how is contraction of muscles initated?

A

Contraction results from the phosphorylation of the regulatory myosin light chain in the presence of elevated calcium and ATP

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9
Q

Simply, how is relaxation of smooth muscles initiated?

A

The dephosphorylation of myosin light chain by myosin phosphatase which has consitutive activity

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10
Q

How is the activity of MLCK and myosin phosphatase regulated?

A

Extracellular signals:

Adrenaline activate a beta2-adrenoceptor which then activated Gs, which then activated cAMP which activated PKA

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11
Q

What can PKA do?

A

Phosphorylate and therefore inhibit MLCK
Phosphorylate and therefore stimulat myosin phosphatase
Causes relaxation of bronchail smooth muscle

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12
Q

What is the mechanism of asthma?

A

Increased mass of smooth muscle (hyperplasia and hypertrophy)
Accumulation of interstitial fluid (oedema)
Increased secretion of mucus
Epithelial damage exposing sensory nerve endings
Sub-epithelial fibrosis

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13
Q

How is the airway narrowed and what can it cause?

A

Inflammation and bronchoconstriction which increases airway restriction and therefore FEV1 and PERF

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14
Q

What is bronchial hyper-responsiveness in asthma due to?

A

Epithelial damage which exposes sensory nenrve endings that contribute to increased sensitivity of the airways to bronchoconstrictor influences and may cause neurogenic inflammation by the release of various peptides from sensory nerve endings

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15
Q

What are the 2 components to asthma?

A

Hypersensitivity

Hyper-reactivity

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16
Q

What test reveals hyper-responsiveness?

A

A provocation test with inhaled bronchoconstrictors (spasmogens) such as histamine or methacholine

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17
Q

What is FEV1?

A

The forced expiatory voluble in liters in one seconds

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18
Q

What is the mechanism in a nonatopic individual when they are exposed to an antigen?

A

The allergen is phagocytosed by dendritic cells which activates a low level TH1 response which is a cell-mediated immune response involving IgG and macrophages

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19
Q

What is the mechanism in an atopic individual when they are exposed to an antigen?

A

It is phagocytosed by dendritic cells but a strong TH2 response is activated which is antibody mediated and involves IgE

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20
Q

What happens in allergic asthma?

A

There is antigen presentatino by CD4+ cells which iduces the clonal expansion and maturation of B cells to IgE secreting plasma cells. This is mediated by interleukins

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21
Q

What happens during the development of allergic asthma?

A

The eosinophils differentiate and activate a response to IL-5 which is released from TH2 cells.

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22
Q

What do the mast cells in airways express?

A

IgE receptors in response to IL-4 and IL-13 released from TH2 cells

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23
Q

What does the cross-linking of IgE receptors stimulate?

A

The entry of calcium into mast cells and the release of calcium from intracellular stores evoking the release of secretory granules containing histamine and the production and release of leukotrines that cause airway smooth muscle contraction

24
Q

What are examples of drugs that relieve asthma by acting as bronchodilators?

A

Short acting beta2-adrenoceptos agonists (SABAs)
Long acting beta2-adrenoceptors agonists (LABAs)
CysLT1 receptor antagonists

25
Q

What are examples of drugs that control/prevent asthma by acting as anti-inflammatory agents?

A

Glucocorticoids - steroids
Cromoglicate - non-steroidal
Humanised monoclonal IgE antibodies

26
Q

What drug can be used as a reliever and preventor?

A

Methylxanthines

27
Q

What are beta2-adrenoceptos antagonists of?

A

All spasmogens

28
Q

What is the general mechanism of beta2-adrenoceptors?

A

The reduction of calcium and potassium channels hyperpolarising the membrane

29
Q

What is an examples of a SABA?

A

Salbutamol

30
Q

What are some characteristics of SABAs?

A

First line in the treatment of an acute, mild asthma attack
Can be taken as needed via inhalation but can be IV in an emergency
Rapid action - within 5 mins and will persist for 3/5 hours

31
Q

What is the action of SABAs?

A

Increases mucus clearance and decreases mediator release from mast cells and monocytes

32
Q

What are the side effects of SABAs?

A 
Can cause:
Tremors
Tachycardia
Cardiac dysrhythmia
Hypokalemia
33
Q

What are examples of LABAs?

A

Salmeterol

Formoterol

34
Q

What are some characteristics of LABAs?

A

NOT recommended for use in acute asthma attacks
Useful for nocturnal asthma
Should always be used in conjunction with glucocortioid

35
Q

What is the mechanism of action of CysLT1 receptors?

A

They are derived from mast cells and infiltrating inflammatory cells that cause smooth muslce conrtaction, mucus secretion and oedema

36
Q

What are some examples of CysLT1 receptors?

A

Montelukast and zafirlukast

37
Q

What are some characteristics of CysLT1 receptors?

A

Effective as an add on therapy against early and late bronchospasms in mild and peprsisten asthma and in combo with other medications
Effective against antigen-induced and exercise-induced bronchospasm
Relaxes smooth muscle in response to CysLTs
Oral route
NOT recommended for releif of acute severe asthma

38
Q

What is the main hormone in glucocorticoids?

A

Cortisol

39
Q

What does cortisol regulate?

A 
Reduces inflammatory response 
Reduces immunological response 
Increases liver glycogen deposition 
Increases gluconegenesis 
Increases glucose output from the liver
Decreases glucose utilization 
Increases protien catabolism 
Increases bone catabolism 
Increases gastic acid and pepsin secretion
40
Q

What is the mechanism to COPD?

A

Smoking (air pollution)
Stimulation of resident alveolar macrophages
Cytokine production
Activation of neutrophils, CD8 T cells, increased macrophage numbers
Release of matrix metalloproteinases (e.g. elastase) and free radicals resulting in chronic bronchitis and emphysema

41
Q

What is the function of Musarinic Acetylcholine (ACh) receptors antagonists in the airways?

A

They reduce the parasympathetic neuroeffector transmission in the airways.

42
Q

What are the different types of muscarinic acetylcholine receptors in the airways?

A

M1, M2 and M3

43
Q

What is the function of M1?

A

Facilitates fast neurotransmission between preganglionic neurons and postganglionic neurones

44
Q

What is the function of M2?

A

Acts as an inhibitory autoreceptor reducing the release of ACh at the
postganglionic neurone
M2 receptors act in a negative feedback manner to reduce the amount of ACh released to the cell. The stimulation of M2 receptors will reduce the release of ACh and therefore if M2 is blocked there is an increase in the release of ACh

45
Q

What is the function of M3?

A

ASM, mediates contraction to ACh - is also present on mucus secreting cells evoking increased secretion.
In the treatment of COPD and asthma, an M3 receptor blocker is used

46
Q

What is the mechanism of SAMAs in treatment of COPD?

A

Slower working than b2 agonists but are more effective, longer lasting and suppress the cough reflex in response to an irritant stimulus. The airways are innervated by sensory neurones, the sensory and motor nerves are both located within the vagus nerve. This is called the vago-vagal reflex. Muscarinic antagonists will stop the final step in the vago-vasal reflex preventing the release of ACh by postganglionic neurones and therefore preventing the cough reflex

47
Q

What is ipratropium?

A

SAMA that is a non-selective blocker of M1, M2 and M3 receptors, preferred agents with some selectivity for M3 are avaliable

48
Q

What does PDE4 do in the treatment of COPD?

A

PDE is expressed in neutrophils, T cells and macrophages and therefore the inhibition of PDE4 has an inhibitory effect upon inflammatory and immune cells

49
Q

What is an example of a PDE4 inhibitor?

A

Rofumilast which suppresses inflammation and emphysema

50
Q

What is rhinitis?

A 
A common disease involving acute or chornic inflammation of the nasal mucosa which is characterized by:
Rhinorrohea
Sneezing
Itching
Nasal congestion and obstruction
51
Q

How can allergic rhinitis be classified?

A

Seasonal (SAR)
Perennial (PAR)
Episodic (EAR)

52
Q

What is the mechanism of allergic rhinitis?

A

Inhalation of allergen increases specific IgE levels
IgE binds to receptors on mast cells and basophils
Re-exposure to allergen causes mast cell and basophil degranulation
Mediators such as histamine, cysLTs, tryptase, prostaglandins causing acute itching, sneezing, rhinorrhoea and nasal congestion
Delayed response caused by recruitment of lymphocytes and eosinophils to nasal mucosa contributes to congestion and obstruction

53
Q

What are the different types of non-allergic rhinitis?

A 
Infection 
Hormonal imbalance 
Vasomotor disturbances 
Non-allergic rhinitis with eosinophilia syndrome 
Medications - drug induced rhinitis
54
Q

What are the targets in the treatment of rhinitis and rhinorrhoea?

A

Anti-inflammatory - glucorticoids
Mediator receptor blockade - H1 receptor antagonists, CysLT receptor antagonists
Nasal blood flow - vasoconstrictors - alpha 1 adrenoceptors
Decongestant
Anti-allergic - sodium cromoglicate

55
Q

What is the mechanism of glucorticoids?

A

Reduce vascular permeability, recruitment and activity of inflammatory cells and release of cytokines and mediators

56
Q

What is the mechanism of Anti-histamines (H1 receptor antagonists)?

A

Competitive antagonists that have the effects of mast cell derived histamine including: Reduces vasodilation and increased capillary permeability
Reduces the activation of sensory nerves
Reduces mucus secretion from submucosal glands

Respiratory (24 decks)

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