pharmacology Flashcards

1
Q

one major cause of asthma

A

due to an immune imbalance between TH1 and TH2 lymphocyte mediated responses

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

asthma definition

A

is a recurrent and reversible obstruction to the airways in response to substances that are not necessarily noxious, normally do not affect non-asthmatic subjects

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

causes of asthma attack

A

allergens - atopic individuals
exercise - cold, dry air
respiratory infections - viral
smoke, dust, environmental pollutants

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

pathological changes in chronic 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

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

bronchial hyper responsiveness

A

epithelial damage exposing sensory nerve endings, contributes to increased sensitivity of the airways to bronchoconstrictor influences and may cause neurogenic inflammation by the release of various peptides

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

TH2 lymphocyte activation

A

involve IgE
activated by TH0, that produce a cytokine environment
TH2 cells activate B cells by binding to them and by IL-4 production

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

role of mast cells

A

cross links IgE receptors
stimulates calcium entry into mast cells release of Ca from intracellular stores evoking
release of secretory granules containing preformed histamine and the production and release of other agents that cause airway smooth muscle contraction
release of substances that attract cels casuing inflammation into the area

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

immediate phase of asthma attack

A

bronchospasm
type 1 hypersensitivity reaction
allergen or non-specific stimulus
mast cells, mononuclear cells

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

delayed phase of an asthma attack

A

inflammatory reaction
type 4 hypersensitivity reaction
infiltration of cytokine releasing TH2 cells and monocytes activation of inflammatory cells - eosinophils

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

stimulation of postganglionic cholinergic fibres causes

parasympathethic

A

bronchial smooth muscle contraction mediated by M3 muscarinic ACh receptors on ASM cells
increased mucus secretion mediated by M3 muscarinic ACh receptors on gland goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

stimulation of postganglionic noncholinergic fibres causes

parasympathetic

A

bronchial smooth muscle relaxation mediated by NO and vasoactive intestinal peptide VIP

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

stimulation of sympathetic causes

A

bronchial smooth muscle relaxation via beta ADR on ASM cells activated by adrenaline released from the adrenal gland
decreased mucus secretion mediated by beta ADR on epithelial cells
vascular smooth muscle contraction mediated by alpha 1 ADR on vascular smooth muscle

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

intracellular calcium

A

elevated Ca rate of phosphorylation exceeds the rate of depolarisation
relaxation requires the return of Ca to basal level achieved by primary and secondary active transport

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

pharmacological management of asthma

A

beta 2 adrenoceptor agonists - bronchodilators

airway smooth muscle relaxation - reduction in intracellular Ca conc and activation of large conductance K channels

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

SABA

A

reliever
salbutamol
first line treatment for mild, intermittent asthma
inhalation, taken as needed, act rapidly
increase mucus clearance and decrease mediator release from mast cells and monocytes
few adverse effects

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

LABA

A
reliever
salmeterol
slow to act 
useful for noctural asthma 
not used as monotherapy 
coadministered with glucocorticoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cysteinyl leukotriene receptor antagonists

A
reliever
montelukast 
act competitively 
derived from mast cells and infiltrating inflammatory cells cause smooth muscle contraction, mucus secretion and oedema 
add on therapy 
effective against antigen-induced and exercise induced bronchospasm 
oral route 
headache and GI upset side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

methylxanthines

A

theophylline
combine bronchodilator and anti-inflammatory actions, inhibit mediator release from mast cells, increase mucus clearance
second line combination with LABA and glucocorticoids
narrow therapeutic values
numerous drug interactions

19
Q

glucocorticoids

A
controllers/preventors
beclometasone, fluticasone, prednisolone 
anti-inflammatory agent 
main hormone is cortisol 
regulates numerous essential processes
inhaled to reduce systemic effects
20
Q

cromoglicate

A

controllers/preventors

21
Q

humanised monoclonal IgE antibodies

A

controllers/preventors
binds IgE via Fc to prevent attachment to Fcz receptors - suppresses mast cell response to allergens
IV
monoclonal antibodies directed against IL-5 - mepolizumab

22
Q

mineralcocorticoids

A

mainly aldosterone
regulate the retention of salt by the kidney
not wanted in inflammatory conditions

23
Q

cromones

A

second line drugs now infrequently used
mast cell stabilizers
no direct effect upon bronchial smooth muscle
weak anti-inflammatory effect

24
Q

chronic bronchitis

A
inflammation of bronchi and bronchioles 
cough 
clear mucoid sputum 
infections with purulent sputum 
increasing breathlessness
25
Q

emphysema

A

distension and damage to alveoli
destruction of acinial pouching in alveolar sacs
loss of elastic recoil

26
Q

COPD pathogenesis

A

smoking/air pollution
stimulation of resident alveolar macrophages
cytokine production
activation of neutrohils CD8 T cells increased macrophage numbers
release of matrix metalloproteinases, free radicals

27
Q

muscarinic acetylcholine receptors in the airways

A

reducing parasympathetic neuroeffector transmission with muscarinic receptor antagonists is an important treatment of COPD

28
Q

muscarinic receptor antagonists

A

pharmacological antagonists of bronchoconstriction caused by smooth muscle M3 receptor activation in response to ACh released from postganglionic parasympathetic fibres

29
Q

M1

A

ganglia

facilitate fast neurotransmission mediated by ACh acting on nicotinic receptors

30
Q

M2

A

postganglionic neurone terminals - act as inhibitory autoreceptors reducing release of ACh - blockage increases release of ACh`

31
Q

M3

A

ASM

mediate contraction to ACh, evoke increased mucus secretion

32
Q

SAMA

A

ipratropium

non-selective blocker of M1 M2 and M3 receptors preferred agents with some selectivity for M3 are available

33
Q

LAMA

A
tiotropium 
glycopyrronium 
aclidinium 
umeclidinium 
have few adverse effects 
mainly palliative 
decrease mucus secretion 
reduce bronchospasm caused by irritant stimuli and also block ACh mediated basal tone
34
Q

PDE4 inhibitor

A

rofumilast

suppresses inflammation and emphysema

35
Q

PDE4

A

is the prominent PDE expressed in neutrophils, T cells and macrophages

36
Q

rhinitis

A

acute or chronic inflammation of the nasal mucosa
rhinorrohea, sneezing, itching, nasal congestion and obstruction
allergic, non-allergic or mixed

37
Q

allergic rhinitis

A

seasonal, perennial, episodic

similarities to allergic asthma and are strongly linked

38
Q

non allergic rhinitis

A

any rhinitis that does not involve IgE dependent events
causes - infection, hormonal inbalance, vasomotor disturbances, nonallergic rhinitis with eosinophilia syndrome NARES, medications

39
Q

occupational rhinitis

A

may involve both allergic and non-allergic components

40
Q

rhinitis and rhinorrhoea

A

involve increased mucosal blood flow increased, blood vessel permeability, increases the volume of nasal mucosa and cause difficulty breathing

41
Q

targets and treatment of rhinitis

A

anti-inlammatory - glucocorticoids
mediator receptor blockade - H1 receptor antagonists, CysLT1 receptor antagonists
nasal blood flow - vasoconstrictors
anti-allergic - sodium cromoglicate

42
Q

anti-histamine

H1 receptor antagonists

A
competitive ntagonists that reduce effects of mast cell derived histamine - vasodilation and increased capillary permeability, activation of sensory nerves, mucus secretion fro submucosal glands 
orally, intranasal spray
azelastine 
effective as a monotherapy 
ioradidine
fexofenadine
cetrizine
43
Q

alpha adrenoceptor agonist

A

decrease swelling in vascular mucosa
vasoconstrictors
oxymetazoline
effective, short-term, in reducing congestion in allergic rhinitis