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Z MD1 Respiratory block > Respiratory disease and their treatment > Flashcards

Respiratory disease and their treatment Flashcards

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1
Q

what mechanisms increase free intracellular calcium

A
  • voltage gated calcium channels - phospholipase C/inositol trisphosphate - releases from intracellular stores
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2
Q

endogenous mediators for airway smooth muscle contraction

A
  • ACh - histamine - Leukotrienes - LTC4 and LTD4
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2
Q

major cytokines of slow response of mast cell activation

A

IL-4, IL-5, GM-CSF

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2
Q

main mediators involved in COPD

A

LTB4, IL-8, TNF-alpha, ROS+++

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3
Q

what effects are controlled with relievers, controllers and preventers

A
  • airway SM bronchoconstriction - treated with relievers, controllers and preventers - bronchial wall oedema and mucus hypersecretion - can only be treated with prenters
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4
Q

what is the action of leukotriene B4

A

promotes inflammation by attracting leukocytes

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5
Q

how is the B2 adrenoceptor downregulated

A
  • decreased mRNA stability - receptor protein degradation - decreased rate of transcription
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6
Q

intrinsic stimuli for mast cell activation

A

C5a neuropeptides osmotic stimuli hypertonic stimuli

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7
Q

main genes turned off with GCS and their actions

A
  • cytokines - inducible enzymes for inflammatory mediators (PLA2, iNOS, COX-2) - adhesion molecules (ICAM-1, E-selectin)
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8
Q

drugs that are LABAs

A

salmeterol - slow onset, 12 hour duration formoterol - rapid onset, 12 hour duration indacaterol - rapid onset, 24 hour duration

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8
Q

mediators in the rapid response of mast cell activation

A

cysteine-leukotrienes and PGD2

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9
Q

what blocks the actions of cysteinyl leukotrienes

A

luekotriene antagonists (monteleukast)

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9
Q

how do GCSs have their effects

A
  • transactivation - activation of anti-inflammatory genes - transrepression - ligand-bound GR engages and inhibits inflammatory genes
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10
Q

when are H1 receptor antagonists indiciated

A
  • uticaria - atopic dermatitis - hayfever - anaphylaxis and angioedema - bites and stings - motion sickness -NOT INDICATED FOR ASTHMA OR COLDS
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10
Q

treatment of PAH

A

endothelin receptor antagonists prostanoids phosphodiesterase inhibitors

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12
Q

what holds the small airways open

A

parenchymal tethering - stretch further opposes shortening of SM

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13
Q

3 classes of H1 receptor antagonists

A

sedative non-sedative (caused long QT) new non-sedative

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13
Q

side effects of oral GCS

A
  • osteoporosis - diabetes - muscle wasting - hypertension - growth suppression - suppression of adrenal/pituitary/hypothalamic axis
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14
Q

definition of asthma

A

a chronic inflammatory disorder of the airways associated with airway hyper-responsiveness

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14
Q

histological changes of an asthmatic epithelial cell

A
  • goblet cell metaplasia - subepithelial collagen thickening of BM - infiltration of inflammatory cells - increased mucosal vascularity - increased smooth muscle volume - epithelial damage
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14
Q

How do SABAs work

A

activate B2 adrenoceptor - activates Gs - stimulates cAMP –> activates PKA: - activates SERCA - inhibits IP3R Leads to reduced cytoplasmic Ca and therefore less MLCK activation

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14
Q

action of muscarinic receptor antagonists

A

prevent manifestations of reflex airway obstruction - less effective than beta-2 agonists

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15
Q

pharmacological inhibitors of mast cell activation

A

disodium cromoglycate nedocromil sodium

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16
Q

side effects of inhaled GCS

A
  • dysphonia -oral candidiasis - decreased serum cortisol
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18
what happens to the B2 adrenoceptor one sequestrated
either dephosphorylated and recycled or degraded and lost
20
drugs that are SABAs
salbutamol terbutaline
21
actions of phosphodiesterase inhibitors
- PDE inhibition - smooth muscle relaxant - adenosine antagonism - HDAC 2 activation
22
how are cysteinyl leukotrienes made
AA --\> 5-HPETE (by 5-lipoxygenase) 5-HPETE --\> LTA4 --\> LTC4 (by glutathione S-transferase)
23
side effects of theophylline
nausea, vomiting, diarrhoea, CNS stimulation, dysrythmias
24
when do you use LABAs on patients
in combination with GCS - used as monotherapy - linked to increased morbidity and mortality
25
main cells involved in asthma
mast cells eosinophils CD4 T cells macrophages
27
extrinsic stimuli for mast cell activation
- allergen (IgE) - polybasic drugs - mechanical stimulation - UV light/heat
28
action of disodium cromoglycate and nedocromil sodium
- only modestly anti-inflammatory - reduction in mast cell degranulation, C-fibre activation and eosionophil activation - cause annexin-1 release --\> resolves inflammation
30
mechanisms decreasing free intracellular calcium
- plasma Ca ATPase - extrusion across the plasma membrane - Sarcoplasmic SERCA - uptake into internal stores
30
when are GCS indicated
- using b2 agonist \>3 times a week - FEV1
31
why do local mediators only act locally?
they are quite labile they are rapidly metabolised close to their site of release
33
what are the inflammatory effects of asthma
- mucus hypersecretion and hyperplasia - vasodilation - plasma leak - oedema - epithelial shedding - bronchoconstriction - SM hypertrophy, hyperplasia - subepithelial fibrosis - sensory nerve activation
33
main cytokines of the delayed phase of mast cell activation
CSF, TNF, chemokines
35
duration of action of SABAs is dependent on
perfusion of the lung - not by metabolism
36
main cells involved in COPD
neutrophils CD8 T cells macrophages +++
38
how is phosphorylation of beta-2 adrenoceptor achieved
by PKA and beta adrenergic receptor kinase - also enhances binding of B-arrestin
38
what produces cysteinyl leukotrienes?
eosinophils, mast cells and macrophages
39
main mediators involved in asthma
LTD4, histamine, IL-4, IL-5, ROS
40
onset of SABAs
rapid - 2-5 minutes
42
mediators in the immediate response of mast cell activation
histamine, heparin, tryptase, TNF-alpha
43
what is the pharmacological treatment for inhibiting mediator production in allergy
glucocorticoids --\> reduce mast cell cytokine production
44
adverse effects of SABAs
tachycardia, tremor, hypokalemia
45
when is pharmacological treatment indicated with pharmacological mast cell activation inhibition
indicated for treatment of allergic responses of mucosal surfaces
46
results of immediate phase of the mast cell responses
- pain and itch (sensory nerve activation) - bronchospasm - mucus secretion - vasodilation - hypotension - increased vascular leak of endothelium - hypovolemia - positive inotropic and chrontropic effects - gastic acid secretion - CNS - increased w
47
when is 5-lipoxygenase activated
by an increase in intracellular Ca by stimuli produced in infection, allergic responses ans other forms of inflammation
49
what types of pharmacological drugs inhibit mediator actions
H1 receptor antagonists cysteinyl leukotriene receptor antagonists
50
what are ITAMS
immunoreceptor Tyrosine-based Activation MotifS
51
result of activation of CysLT1 R
- hypotension during anaphylactic shock - vasodilator in skeletal muscle - decreased CO - hypovolaemia - airway obstruction in asthma - nasal obstruction in hayfever
52
3 phases of mast cell responses
- immediate - rapid - slow
54
where does LTC4 and metabolites act
on Cys-LT1 Receptor
54
action of cysteinyl leukotriene receptor antagonists
bronchodilation
55
4 targets for anti-allergic drugs
- inflammatory cell activation - mediator production - mediator action - prevention and desensitisation
56
regulation of airway smooth muscle contraction performed by
- protein kinase A - activates myosin light chain phosphatase - Rho kinase - inhibits myosin light chain phosphatase - protein kinase c - inhibits myosin light chain phosphatase
57
examples of cysteinyl leukotriene receptor antagonists
zafirlukast montelukast
58
what are examples of muscarinic receptor antagonists used in asthma
ipratropium bromide - non selective tiotropium bromide - M3 selective
59
regulation of beta-2 adrenoceptors achieved by: (3)
- phosphorylation (seconds) - sequestration (minutes) - downregulation (hours)
61
endogenous inhibitors of mast cell activation
PGE2 adrenaline crotisol
63
cysteinyl leukotriene receptor antagonists indicated for
- aspirin-induced asthma - exercise-induced asthma - combination therapy - allergic rhinitis
64
endogenous mediators for airway smooth muscle relaxation
- adrenaline - PGE2 - PGI2
65
main genes turned on with GCS and their actions
B2-adrenoceptor - more Rs to initiate SM contraction Annexin-1 - anti-inflammatory serpin A3 - inhibitor of serum proteases
66
drugs that are phosphodiesterase inhibitors
theophylline roflumilast
67
actions of glucocorticoids in asthma
reductions in: - activity, recruitment and survival of eosinophils and T lymphocytes - activation of mast cell and macrophage cytokine production - in proliferation, cytokine and collagen production by smooth muscle and fibroblasts LEADS TO DECREASE INFLAMMATORY CELL NUMBER AND ACTIVATION
68
mechanism of airways SM bronchoconstriction
increase in calcium -\> binds to calmodulin -\> activates myosin light chain kinase to phosphorylate myosin light chain -\> activation of actomyosin ATPase --\> myosin- actin crosslinking and contraction
69
what is the purpose of the slow response of the mast cell response
to set up the environment for infiltration of eosinophils, more mast cells and prolonged survival of these cells

Z MD1 Respiratory block (11 decks)

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