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The respiratory system > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What does stimulation of postganglionic cholinergic fibres cause?

A
  • broncial smooth muscle contraction mediated M3 muscarinic ACh receptors on ASM cell
  • increased mucus secretion mediated by M3 muscarinic Act receptors on gland cells
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2
Q

What does stimulation of postganglionic noncholinergic fibres cause?

A
  • bronchial smooth muscle relaxation mediated by Nitric oxide and vasoactive intestinal peptide
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3
Q

What does post ganglionic stimulation in the sub mucosal glands and smooth muscle of the blood vessels cause?

A
  • bronchial smooth muscle relaxation via B2 adrenoceptors on ASM cells activated by adrenaline released from adrenal gland
  • decreased mucous secretion
  • increased mucocilary clearance
  • vascular smooth muscle contraction
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4
Q

describe the initiation of contraction by Ca2+ in smooth muscle?

A
  • rise in cytoplasmic Ca2+
  • interacts with calmodulin
  • activating MLCK
  • drives movement of myosin and actin across each other
  • causes cell to contract
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5
Q

How does relaxation of smooth muscle occur?

A

It results from the dephosphorylation of MLC by myosin phosphatase

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6
Q

Describe the pathological changes that occur in asthma?

A
  1. increased mass of smooth muscle
  2. accumulation of interstitial fluid
  3. increased secretion of mucous
  4. epithelial damage
  5. sub - epithelial fibrosis
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7
Q

Describe the phases of an asthma attack

A
  • type 1 hypersensitivity reaction: early phase, bronchospasm and acute inflammation
  • type 2 hypersensitivity: late phase: bronchospasm and delayed inflammation
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8
Q

Describe the immune reaction to an allergen in an atopic individual?

A

Allergen > phagocytosis > strong Th2 response, antibody mediated immune response involving IgE

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9
Q

What do cross liked IgE receptors do?

A
  • stimulates calcium entry into mast cells (degranulation)

- simulates release of calcium from intracellular stores (inflammation)

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10
Q

What are relievers in the treatment of asthma?

A
  • act as bronchodilators
  • SABAs
  • LABAs
  • CysLT1 receptor antagonists
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11
Q

what are controllers in the prevention of asthma?

A
  • act as anti inflammatory agents that reduce airway inflammation
  • glucocorticoids
  • cromoglicate
  • IgE antibodies
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12
Q

SABA B2 adrenoceptor agonists

A
  • salbutamol
  • relievers taken as needed
  • administered via inhalation
  • act rapidly
  • increase mucous clearance and decrease mediator release from mast cells and monocytes
  • few side effects
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13
Q

LABA B2 adrenoceptor agonists

A
  • salmeterol, formoterol
  • not for acute relief of bronchospasm
  • useful for nocturnal asthma
  • can be used as add on therapy with glucocorticoid
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14
Q

CysLT1 receptor antagonists

A
  • montelukast, zafirlukast
  • add on therapy against early and late bronchospasm in mild asthma
  • relax bronchial smooth muscle in response to cysLTs
  • oral administration
  • side effects: headache, GI upset
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15
Q

Xanthines

A
  • methylxanthines
  • combine bronciodilator and anti inflammatory actions
  • administered orally
  • very narrow therapeutic window
  • many adverse side effects
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16
Q

what are synthetic derivatives of cortisol used for?

A
  • they are used for their anti inflammatory effects in the treatment of asthma
  • delivered via inhalation
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17
Q

describe the mechanism of action of glucocorticoids?

A
  • signal via nuclear receptors (GRa)
  • combine with GRa and produce inhibitory heat shock proteins
  • activated receptor monomers assembled to homodimers and bind to GRE
  • transcription of genes is either switched on or off
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18
Q

What glucocorticoid is given in severe/rapidly deteriorating asthma?

A
  • oral predinisolone combination with inhaled steroid
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19
Q

What are cromones?

A
  • second line drugs infrequently used prophylactically in the treatment of allergic asthma
  • delivered by inhalation
  • can reduce both phases of an asthma attack
  • more effective in children
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20
Q

Describe the role of muscarinic receptor antagonists in COPD?

A

They act as pharmacological antagonists of bronchoconstriction caused by smooth muscle M3 activation in response to ACh released from post ganglionic parasympathetic fibres

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21
Q

describe the mechanism of COPD?

A

smoking causes the stimulation of resident alveolar macrophages which promotes cytokine production and activation of neutrophils, CD8 T cells and increased macrophage numbers. metalloproteins and free radicals are then released which leads to chronic bronchitis/emphysema

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22
Q

what are the characteristics of chronic bronchitis?

A
  • inflammation of bronchi and bronchioles
  • cough
  • clear mucoid suptum
  • infections with purulent sputum
    increasing breathlessness
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23
Q

What are the characteristics of emphysema

A
  • distension and damage to alveoli
  • destruction of acing pouching in alveolal sacs
  • loss of elastic recoil
24
Q

how does the expiration phase differ in a patient with COPD

A

much greater resistance to airflow during expiration

25
Q

Where is the M1 receptor located?

A

Ganglia

26
Q

where is the M2 receptor located?

A

post ganglionic neurone terminals

27
Q

where is the M3 receptor located?

A

airway smooth muscle

28
Q

What are the muscarinic receptor antagonists used in the treatment of COPD?

A
  • ipratropium
  • Tiotropium
  • Glycopyrronium
  • Aclidinium
  • Umeclidinium
29
Q

how do LABA/LAMA combinations work in the treatment of COPD

A

Drugs work by different but complementary mechanisms to cause smooth muscle relaxation
combinations are most effective when both drugs are deposited in the same location

30
Q

What is Rhinitis

A
  • acute or chronic inflammation of the nasal muscosa
31
Q

Describe allergic rhinitis?

A

allergen triggers mast cell and basophil degranulation which stimulates the release of histamine, cysLT ect which causes the symptoms

32
Q

What is non allergic rhinitis?

A

Any rhinitis, acute or chronic that doesn’t involve IG5 dependent events
many different causes including infection and hormone imbalance

33
Q

What is occupational rhinitis?

A

May involve both allergic and non allergic components

34
Q

How are glucocorticoids used in the treatment of rhinitis?

A
  • reduce vascular permeability, recruitment and activity of inflammatory cells and the release of cytokines and mediators
35
Q

Give examples of the glucocorticoids used in the treatment of rhinitis?

A
  • beclometasone
  • fluticasone
  • prednisolone (oral)
36
Q

How are anti histamines used in the treatment of rhinitis?

A

they are competitive antagonists that reduce the effects of mast cell derived histamine

37
Q

give examples of antihistamines used in the treatment of rhinitis?

A
  • loradtidline
  • fexofenadine
  • cetirizine
38
Q

How are anti cholinergic drugs used in the treatment of rhinitis?

A
  • ACh released from post ganglionic parasympathetic fibres activates muscarinic receptors on nasal glans causing a watery secretion that contributes to rhinnorhoea - this mechanism is blocked by muscarinic antagonists (ipratropium)
39
Q

How are cysteinyl leukotrine receptor antagonists used in the treatment of rhinitis?

A

CysLT1 receptor antagonists reduce the effects of CysLTs upon the nasal mucosa
- montelukast

40
Q

how are vasoconstrictors used in the treatment of rhinitis?

A
  • mimic the effect of noradrenaline.
    produce vasoconstriction via activation of alpha1 adrenoceptors to decrease swelling in the vascular mucosa
  • oxymetazoline
41
Q

What are the BTS asthma guidelines?

A
  • short acting B2 agonists as needed
  • inhaled steroids
    • LABA/LAMA + LTRA/theo/cromone
    • oral steroid + anti IgE/anti IL5/anti IL4a
42
Q

what are the actions of a spacer device?

A
  • avoids coordination problems
  • reduces oropharyngeal and laryngeal side effects
  • reduces systemic absorption
  • reduces particle size and velocity
  • improves lung disposition
43
Q

describe the anti inflammatory action of cromones?

A
  • only used in asthma
  • mast cell stabiliser - weak inflammatory cf steroids
  • inhaled route only
44
Q

describe the use of leukotriene receptor antagonists?

A
  • used in asthma
  • anti inflammatory
  • 2nd line = complementary non steroidal anti inflammatory additive to inhaled steroid
  • also used in allergic rhinitis
45
Q

describe the use of montelukast?

A
  • leukotriene receptor antagonist
  • oral route
  • 1x daily
  • high therapeutic ratio
46
Q

describe the mechanism of anti IgE monoclonal antibody (omalizumab)?

A
  • inhibits the binding to the high affinity IgE receptor - inhibits TH2 response and associated mediator release from basophils/mast cells
47
Q

describe the mechanism of anti-IL5 (mepolizumab)?

A
  • blocks the effect of the TH2 cytokine IL5 which is responsible for eosinophilic inflammation in asthma
48
Q

Describe the mechanism of anti IL4a (dupilumab)?

A
  • blocks the effects of the TH2 cytokines IL4/13 which is responsible for eosinophilic inflammation, IgE, airway hyperreactivity and mucin production in asthma
  • suppresses IgE and FeNO
49
Q

salbutamol

A
  • bronchodilator
  • B2 agonist
  • SABA
50
Q

What is the mechanism of muscarinic antagonist bronchodilators?

A
  • block post junctional end plate M3 receptors
  • inhaled only
  • high therapeutic ratio
51
Q

Roflumilast

A
  • PDE4 inhibitor
  • oral tablet
  • indicated for COPD only
  • minimal effect of FEV1 (anti inflammatory)
  • used as additive with LABA/LAMA
52
Q

What are mucolytics?

A
  • reduce sputum viscosity and aide sputum expectoration in COPD
  • oral carbocisteine, erdosteine
  • only used as an add on
53
Q

Describe the treatment of chronic asthma?

A
  • suppress inflammatory cascade (inh steroid)
    • non steroid anti inflammatory therapy (e.g. theophylline, anti leukotriene cromoglycate)
  • +/- stabilise smooth muscle with LABA/LAMA
54
Q

Describe the treatment of acute asthma?

A
  • oral prednisolone
  • nebulised high dose salbutamol (+/- Neb ipratropium or IV aminophylline/magnesium)
  • at least 60% O2
  • ITU assisted mechanical intubated ventilation if failing paO2 and rising PaCO2
55
Q

describe the treatment of COPD?

A
  • smoking cessation
  • immunisation
  • pharmacotherapy
  • pulmonary rehab
  • oxygen
56
Q

describe the treatment of acute COPD?

A
  • neb salbutamol + ipratropium
  • oral prednisolone
  • antibiotic if infection
  • 24-28% O2 titrated against PaO2/PaCO2
  • physio to aide sputum expectoration
  • non invasive ventilation
  • ITU intubated assisted ventilation only if reversible component

The respiratory system (13 decks)

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