Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y1 Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where are the cell bodies of postganglionic fibres in the parasympathetic innervation to the airways

A

Embedded in the walls of the bronchi and bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the parasympathetic innervation to airway smooth muscle occur (Cholinergic)

A

ACh stimulates M3 receptors on the bronchial smooth muscle leading to contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does parasympathetic innervation to the goblet cells work

A

ACh stimulates M3 receptors on gland cells leading to increased mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the parasympathetic innervation to the airway smooth muscle occur (Non-cholinergic)

A

ACh stimulates the noncholinergic ganglion by NO and VIP to cause smooth muscle leading to relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the sympathetic innervation of the airways occur

A

There is no direct innervation of bronchial smooth muscle in humans
The adrenal glands are stimulated by the sympathetic nervous system, this causes adrenaline release into the blood which stimulates beta-2 adrenoreceptors leading to smooth muscle relaxation, decreased mucus secretion and increased action of the mucociliary clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the general mechanism of excitation-contraction coupling in smooth muscle

A 
A GPCR (M3 for parasymapthetic) leads to formation of IP3 from PIP2.
IP3 causes Ca release from IP3 receptor iron channels  in the sarcoplasmic reticulum.
Ca cause more Ca release by Ca-activated-Ca channels (ryanodine receptors) on the sarcoplasmic reticulum.

Ca can also be moved into the cell by voltage activated Ca channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does Ca cause contraction of the smooth muscle

A

Ca binds to calmodulin.
Ca-Calmodulin causes activation of myosin light chain kinase.
Active MLCK causes phosphorylation of the myosin cross bridge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does relaxation of the smooth muscle occur.

A

Relaxation occurs by the dephosphorylation of myosin light chain by myosin phosphatase.
Reduced levels of intracellular Ca leads to increased myosin phosphatase activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do extracellular signals affect the activity of myosin light chain kinase

A

Adrenalin stimulates GPCR (B2-adrenoceptors) to stimulate adenylyl cyclase to form cAMP.
Raised intracellular cAMP leads to increased activity of protein kinase A.
Protein kinase A phosphorylates MLCK to inhibit it.
Protein kinase A phosphorylates and stimulates myosin phosphatase to reduce phosphorylation of the myosin light chain
These 2 actions result in relaxation of the smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 5 pathophysiological hallmarks of long-standing inflammation due to asthma.

A 
Smooth muscle hypertrophy & hyperplasia
Interstitial oedema
Increased mucosal secretion
Epithelial damage
Sub-epithelial fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the mechanism of bronchial hyper-responsiveness in asthma

A

Epithelial damage leads to exposure of nerve endings
This leads to hypersensitivity in which low level stimulus will cause a bronchial constictive response.
This leads to hyper-reactivity in which a stimulus will produce a larger response than it would in a non asthmatic individual.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which type of T cell dominantes the asthmatic reaction

A

TH2 which leads to a hyper immune response involving IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the mechanism of B cell activation in asthma

A

A proccessed antigen is presented by MHC-II by epithelial cells.
This stimualtes a CD4+ T cell to form TH0 cells which preferntially form TH2 cells.
TH2 stimualte B cells by IL4
Stimualted B cellsmature to IgE plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Expalin the stimultion of mast cells in asthma

A

IgE from plasma cells binds to FcE receptors on the mast cells, this stimualtes Ca influx
TH2 cells produce IL-4&13 which stimulate the mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Expalin the stimulation of eosinophils in asthma

A

IgE from plasma cells bind to FcE receptors on the eosinophils
TH2 cells produce IL-5 which stimualtes the eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the effect of mast cells in asthma

A

Ca influx due to IgE binding to FcE receptors leads to release of secretory granules containing preformed histamines and other agents that cause airway smooth muscle contraction
These chemicals include chemotaxic agents and spasmogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain the difference between the early and late stages of asthma exacerbation

A

Early stage: mast cell degranualtion of preformed products causing bronchospasm and early inflammation

Late stage: Infiltration of cytokine releasing TH2 cells and monocytes leads to activation of inflammatory cells in particular eosinophils

18
Q

Explain the mechanism of B2-adrenoceptor agonists

A

Act as physiological antagonsits of all spasmogens.
Stimulate the B2 receptors (GPCR) leading to activation on adenyl cyclase and increased intracellualr concentrations of cAMP.
cAMP stimulates protein kinase A leading to phosphorylation of MLCK (inhibitory) and myosin phosphatase (stimulatory)

19
Q

Which asthma drug must never be given as monotherapy

A

LABA’s must always be coadministered with a ICS

20
Q

Explain the mechanism of action of CysLT1 receptor antagonsits

A

Act as antagonsits to the CysLT1 receptors which are stimualted by Cystic leukotrines (LTC4, LTD4 and LTE4) to reduce the bronchoconstircor effect of mast cell degranulation.

21
Q

Explain the mechansim of methyxanthines

A

Mechanism not totally understood
Expected theory works off inhibition of phosphodiesterase leading to reduced cAMP breakdown and inturn increased intracellular cAMP concentrations

22
Q

Explain the mechanism of corticosteorids (ICS)

A

These have no direct bronchodialtor action, thus innefective at relief of bronchospasm when given acutely.

Glucocorticoids are lipophilic molecules and enter cells by diffusion across the plasma membrane.
In the cytoplasm they bind to GRa to produce dissocaiton of inhibitory heat shock protiens and are imported to the nucleus by importins.
The monomers assemsble to homodimers and bind to the glucocorticoid response element of certain genes.
This switches on or off genes and modulates the release of proteins (reducing the immune effect)

23
Q

What are the main side effects of B2-adrenoceptor agonists

A

Fine termor commonly

Tachycardia, cardiac dysrhythmia and hypokalaemia can occur less commonly

24
Q

What are the side effects of methylxanthines

A

dysrhythmia, seizure and hypotention all possible if too high a dose
Nausea, vomitng, abdominal discomfort and headaches are common

25
Q

What are the side effects of glucocorticoids

A

Dysphonia

Oropharyngeal candidiasis

26
Q

Explain the mechanism of cromones

A

A weak anti-inflamatory effect

Decrease in the sensitivity of irritant receptors and sensory C-fibres

27
Q

Explain the mechanism of MABs

A

Bind to aspects of the asthma pathway
Omalizumab binds to IgE to stop FcE activation
Mepolizumab binds to IL-5 to reduce eosinophil activation

28
Q

Explain the basic pathway leading to COPD.

A

The activation of neutrophils, CD8+ T cells and, macrophages by cytokines due to the repeated insult of alveolar resident macrophages causes a release of metalloproteases and free radicles.

This causes chronic bronchitis by chronic inflammation and eventual remodelling of the bronchioles.
This causes emphysema by distention and damage along with the destruction of acinial pouching in the alveolar sacs, along with the loss of the elastic recoil.

29
Q

Explain the location and function of the 3 classes of muscarinic receptors within the airway

A

M1 receptors are present on the postganglion neurone and facilitate the fast neurotransmission from the preganglionic fibre

M2 receptors are present at the postpanglionic neurone terminals, these act as inhibiotry autoreceptors reducing the release of ACh (blockage of them increases ACh)

M3 present on the ASM cells themselves. M3 meidate the contraction of the airway by GPCR action.

(Hence why selective M3 receptor agonsits are used)

30
Q

Explain the action of muscarinic receptor antagonists

A

Act as antagonists to M3 receptors (all but ipratroium) reducing the influx of Ca and inturn reducing the effect of MLCK to reduce the levels of contraction.

31
Q

Which is the blockage of M2 receptors non-desirable in the management of COPD.

A

As M2 receptors act as auto-receptor antagonsits.

They reduce the release of ACh to act on M3 receptors

32
Q

What are the 3 classifications of allergic rhinitis

A

Seasonal (related to seasons)
Perennial (present all year)
Episodic (related to a certain thing)

33
Q

Explain the pathway leading to allergic rhinitic

A

An allergen increases levels of allergen-specific IgE
IgE binds to mast cells and basophil FcE receptors
Re-exposure causes mast cell and basophil degranulation
The products of degranulation leads to symptoms both immediate and delayed

34
Q

Explain the main diffrence between allergic and non-allergic rhinitis

A

Allergic rhinits involves IgE, non-allergic does not this occurs by other mechanisms.

35
Q

Explain the mechanism of glucocorticoids in reference to rhinitis

A

Reduce vascualar permiability

Reduce recruitment and activation of pro-inflamatory cells

36
Q

Explain the mechanism of anti-histamines in reference to rhinitis

A

Act as competitive antagonists to H1 receptors to reduce the effect of mast cell-derived histamine
Better for allergic rhinitis

37
Q

Give examples of H1 receptor antagonsits

A

Loratidine, fexofenadine and cetirizine (they end in “ine”)

38
Q

Which anti-cholinergic drug is used in rhinnitis

A

Ipratropium

39
Q

Explain the mechanism of sodium cromoglicate

A

Suspected to stablise mast cells and reduce degranualtion

40
Q

Explain the mechanism of vasoconstirctors (rhinitis)

Give the name of the vasoconstirctor used in rhinitis

A

Act either directly or indirectly to mimic the efect of noradrenalin on a1-adrenoceptors to decreases swelling in th evascular mucosa

Oxymetazoline is a selective a1-adrenoceptor agonsit given for short term relief of allergic rhinitis

41
Q

Explain why oxymetazoline (vasoconstirctor) isn’t recomended for more than a few days

A

Runs the risk of the development of a rebound increase in nasal congestion upon discontinuation
This is due to downregulation and desensitization of receptors in the nasal mucosa.

Y1 Respiratory (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions