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

Respiratory disease and their treatment Flashcards

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
Q

what happens to the B2 adrenoceptor one sequestrated

A

either dephosphorylated and recycled or degraded and lost

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20
Q

drugs that are SABAs

A

salbutamol terbutaline

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21
Q

actions of phosphodiesterase inhibitors

A
  • PDE inhibition - smooth muscle relaxant - adenosine antagonism - HDAC 2 activation
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22
Q

how are cysteinyl leukotrienes made

A

AA –> 5-HPETE (by 5-lipoxygenase) 5-HPETE –> LTA4 –> LTC4 (by glutathione S-transferase)

23
Q

side effects of theophylline

A

nausea, vomiting, diarrhoea, CNS stimulation, dysrythmias

24
Q

when do you use LABAs on patients

A

in combination with GCS - used as monotherapy - linked to increased morbidity and mortality

25
Q

main cells involved in asthma

A

mast cells eosinophils CD4 T cells macrophages

27
Q

extrinsic stimuli for mast cell activation

A
  • allergen (IgE) - polybasic drugs - mechanical stimulation - UV light/heat
28
Q

action of disodium cromoglycate and nedocromil sodium

A
  • only modestly anti-inflammatory - reduction in mast cell degranulation, C-fibre activation and eosionophil activation - cause annexin-1 release –> resolves inflammation
30
Q

mechanisms decreasing free intracellular calcium

A
  • plasma Ca ATPase - extrusion across the plasma membrane - Sarcoplasmic SERCA - uptake into internal stores
30
Q

when are GCS indicated

A
  • using b2 agonist >3 times a week - FEV1
31
Q

why do local mediators only act locally?

A

they are quite labile they are rapidly metabolised close to their site of release

33
Q

what are the inflammatory effects of asthma

A
  • mucus hypersecretion and hyperplasia - vasodilation - plasma leak - oedema - epithelial shedding - bronchoconstriction - SM hypertrophy, hyperplasia - subepithelial fibrosis - sensory nerve activation
33
Q

main cytokines of the delayed phase of mast cell activation

A

CSF, TNF, chemokines

35
Q

duration of action of SABAs is dependent on

A

perfusion of the lung - not by metabolism

36
Q

main cells involved in COPD

A

neutrophils CD8 T cells macrophages +++

38
Q

how is phosphorylation of beta-2 adrenoceptor achieved

A

by PKA and beta adrenergic receptor kinase - also enhances binding of B-arrestin

38
Q

what produces cysteinyl leukotrienes?

A

eosinophils, mast cells and macrophages

39
Q

main mediators involved in asthma

A

LTD4, histamine, IL-4, IL-5, ROS

40
Q

onset of SABAs

A

rapid - 2-5 minutes

42
Q

mediators in the immediate response of mast cell activation

A

histamine, heparin, tryptase, TNF-alpha

43
Q

what is the pharmacological treatment for inhibiting mediator production in allergy

A

glucocorticoids –> reduce mast cell cytokine production

44
Q

adverse effects of SABAs

A

tachycardia, tremor, hypokalemia

45
Q

when is pharmacological treatment indicated with pharmacological mast cell activation inhibition

A

indicated for treatment of allergic responses of mucosal surfaces

46
Q

results of immediate phase of the mast cell responses

A
  • 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
Q

when is 5-lipoxygenase activated

A

by an increase in intracellular Ca by stimuli produced in infection, allergic responses ans other forms of inflammation

49
Q

what types of pharmacological drugs inhibit mediator actions

A

H1 receptor antagonists cysteinyl leukotriene receptor antagonists

50
Q

what are ITAMS

A

immunoreceptor Tyrosine-based Activation MotifS

51
Q

result of activation of CysLT1 R

A
  • hypotension during anaphylactic shock - vasodilator in skeletal muscle - decreased CO - hypovolaemia - airway obstruction in asthma - nasal obstruction in hayfever
52
Q

3 phases of mast cell responses

A
  • immediate - rapid - slow
54
Q

where does LTC4 and metabolites act

A

on Cys-LT1 Receptor

54
Q

action of cysteinyl leukotriene receptor antagonists

A

bronchodilation

55
Q

4 targets for anti-allergic drugs

A
  • inflammatory cell activation - mediator production - mediator action - prevention and desensitisation
56
Q

regulation of airway smooth muscle contraction performed by

A
  • protein kinase A - activates myosin light chain phosphatase - Rho kinase - inhibits myosin light chain phosphatase - protein kinase c - inhibits myosin light chain phosphatase
57
Q

examples of cysteinyl leukotriene receptor antagonists

A

zafirlukast montelukast

58
Q

what are examples of muscarinic receptor antagonists used in asthma

A

ipratropium bromide - non selective tiotropium bromide - M3 selective

59
Q

regulation of beta-2 adrenoceptors achieved by: (3)

A
  • phosphorylation (seconds) - sequestration (minutes) - downregulation (hours)
61
Q

endogenous inhibitors of mast cell activation

A

PGE2 adrenaline crotisol

63
Q

cysteinyl leukotriene receptor antagonists indicated for

A
  • aspirin-induced asthma - exercise-induced asthma - combination therapy - allergic rhinitis
64
Q

endogenous mediators for airway smooth muscle relaxation

A
  • adrenaline - PGE2 - PGI2
65
Q

main genes turned on with GCS and their actions

A

B2-adrenoceptor - more Rs to initiate SM contraction Annexin-1 - anti-inflammatory serpin A3 - inhibitor of serum proteases

66
Q

drugs that are phosphodiesterase inhibitors

A

theophylline roflumilast

67
Q

actions of glucocorticoids in asthma

A

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
Q

mechanism of airways SM bronchoconstriction

A

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
Q

what is the purpose of the slow response of the mast cell response

A

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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