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Pharmacology > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

1
Q

How do beta 2 adrenoceptor agonist reduce histamine release?

A

-Histamine release involves influx of Ca2+ ions.
-A raised cAMP reduces the permeability of cell membranes to Ca2+ ions.
-Beta 2 adrenoceptor agonists stimulate cAMP synthesis
=reduces histamine release

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2
Q

What causes bronchoconstriction?

A

Result from release of ACh, histamine & inflammatory mediators

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3
Q

When you are ‘run down’ what happens to your WBCs?

A

The stress hormone cortisol inhibits WBCs & reduce inflammation causing you to become ill.

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4
Q

What is the effect of histamine causing vasodilation to occur?

A

The release of histamine causes vasodilation on local tissues. This vasodilation is needed to release WBCs (they can now move through the gaps in the capillaries created from vasodilation)

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5
Q

What number is the vagus nerve?

A

Number 10

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6
Q

What does ipratropium bromide do?

A

It’s an anti musclarinic. It inhibits the parasympathetic nervous system, causing bronchodilation.

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7
Q

Why are antihistamines e.g. IV periton used for heart burn?

A

There are H2 receptors in the stomach, which produces HCL, which can cause heart burn.

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8
Q

What is the effect of adrenaline?

A

Works on beta 2 receptors, causing bronchodilation & vascoconstriction.

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9
Q

Why can oedemisis of the larynx occur as a result of shock?

A

Shock is an inadequate tissue perfusion due to a lowering of BP. You can lose a lot of fluid out of blood vessels, go into shock. Can have oedema of airways, as fluid accumulates around larynx (oedemisis tissue around larynx & stop breathing).

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10
Q

What is the effect of prolonged exposure to airway irritants?

A

Chronic inflammation

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11
Q

What is the main side effect of corticosteroids esp preventer inhalers e.g. beclamethasone

A

Oral thrush (candidiasis of mouth)

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12
Q

Name a preventer & reliever inhaler.

A
  • Preventer (brown)- beclamethasone. It prevents inflammation from taking place or keeps inflammation under control.
  • Reliever (blue) (short-acting bronchodilators) -ventalin
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13
Q

What type of drug is prednisolone?

A

Oral steroids

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14
Q

What enables you to breath out?

A

Lung elasticity

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15
Q

What would a sign be that a person has lost the elasticity in there lungs?

A

Use of accessory muscles; costal recession, tracheal tug, supraclavicular recession & abdominal breathing

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16
Q

What is lung compliance?

A

The elasticity of the lungs

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17
Q

What causes loss of the tissue contributing to elasticity?

A

Smoking & long term exposure to irritants

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18
Q

What does airway inflammation cause?

A
  • hyper secretion of mucus
  • airway muscle constriction (bronchoconstriction)
  • swelling of bronchial membranes
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19
Q

What does a spirometery do?

A

Measures lung volume & capacity

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20
Q

What does FEV stand for?

A

Forced expiratory volume

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21
Q

What is a symbicort turbuhaler?

A

Combination of anti inflammatory & bronchodilator

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22
Q

What’s another name for ipratropium bromide?

A

Atrovent

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23
Q

What is chronic bronchitis?

A
  • A condition caused by chronic respiratory irritation, inflammation
  • characterised by increased secretions & infection
  • expectorate (cough up) = green mucus & temp - ?chest infection ?pneumonia
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24
Q

How is emphysema characterised?

A

Characterised by destruction of alveoli, laboured respiratory gas exchange & SOB

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25
Q

What is asthma?

A
  • An inflammatory disease if respiratory passageways

- characterised by bronchoconstriction, SOB & wheezing

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26
Q

What is extrinsic asthma?

A

If the attack has an ALLERGIC basis

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27
Q

What is INTRINSIC asthma?

A

If there is NO allergic basis.

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28
Q

What are the 4 inflammatory mediators of the respiratory tract?

A
  • histamine
  • prostaglandins & leukotrienes
  • eosinophilic chemotactic factor of anaphylaxis (ECF-A)
  • slow reacting substance of anaphylaxis (SRS-A)
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29
Q

How is bronchiolar smooth muscle relaxed?

A

Stimulation of beta-2 adrenergic receptors.

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30
Q

How is bronchiolar smooth muscle contracted?

A

Stimulation of cholinergic receptor (musclarinic)

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31
Q

What does cholinergic mean?

A

A nerve cell where ACh is the NT

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32
Q

What receptor stimulation causes respiratory secretions to increase? What drug can be used to reduce this?

A

Cholinergic stimulation (ACh)

Ipratropium bromide can be used to help reduce respiratory secretions.

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33
Q

Drugs that increase intracellular levels of cyclic AMP produce what?…

A

Bronchodilation

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34
Q

What are 3 bronchodilator drugs?

A
  • sympathomimetics
  • xanthine derivatives
  • parasympatholytics
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35
Q

What are sympathomimetics?

A
  • drugs that partially or completely MIMIC the action of NA or adrenaline
  • act DIRECTLY on alpha &/or BETA adrenoceptor or INDERECTLY on presynpatic terminals, usually by causing a release of NA

E.g. salbutamol (stimulates beta-2 adrenergic receptors)

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36
Q

How does activation of beta-2 adrenergic receptors cause relaxation of smooth muscle?

A

Activation of beta 2 adrenoceptors increases intracellular cAMP, which activates protein kinase. This inhibits muscle contraction by phosphorylation & inhibiting myosin-light-chain kinase.

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37
Q

What are xanthine derivatives?

A

Either used in combo with anti inflammatory or if asthma is resistant to other drugs.
:( has lots of side effects e.g. nausea, headache, insomnia & abdo discomfort

E.g. theophylline

  • inhibits the enzyme phosphodiesterase, so prevents breakdown of cyclic AMP levels in smooth muscle of airways =relaxation of smooth muscles
  • inhibits chemical mediators from being released from mast cells.
  • in COPD, it decreases secretions + stimulates resp
  • overdose causes cardiac and CnS stimulation and can cause seizures

Also…

  • increase adrenaline secretion
  • stimulate heart. Cause vasodilation in most blood vessels
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38
Q

What are parasympatholytics?

A

Drugs that block cholinergic receptors (anticholinergic), musclarinic receptors at bronchioles = bronchodilation and decreases resp secretions

E.g. ipratropium is a musclarinic antagonist

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39
Q

Why shouldn’t asthmatics take paracetamol or ibuprofen?

A

They can cause bronchoconstriction

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40
Q

How do corticosteroids work?

A

Act on immune system by blocking production of substances that trigger allergies and inflammatory actions e.g. prostaglandins. Also prevent function of WBCs (this can cause a side effect of increased susceptibility to infection).

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41
Q

The adrenal cortex releases servers steroid hormones into circulation. These are divided into 2 classes….

A
  • mineralocortocoids - mainly aldosterone- have salt retaining activity
  • glucocorticoids -mainly cortisol (hydrocortisone) - affects carbohydrate & protein metabolism
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42
Q

Give examples of indirectly acting sympathomimetics.

A
  • amphetamines
  • cocaine - inhibits reuptake of NA by nerve terminals
  • They displace NA from its storage vesicles, causing its release from nerve endings
  • inhibit action of MAO
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43
Q

What role does beta adrenergic drugs have on labour?

A

They are used to relax uterine muscle to prevent preterm labour.
E.g. ritodrine

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44
Q

What are beta 1 receptors used for?

A

-found mostly in heart, also located on fat cells, sphincters + smooth muscle of GI tract + renal arterioles

Stimulation leads to…

  • used to stimulate the force of heart contraction in low-output heart failure, heart rate, conduction, contraction and ejection fraction of heart
  • decreased digestion + intestinal motility
  • increased lipolysis in adipose tissue leading to increased blood lipids
  • increases release of renin into renal blood (leads to formation of angiotensin II - vascoconstrictor)
  • beta 1 receptors have an equal affinity for both adrenaline + NA
  • Beta 1-adrenoceptor agonist e.g. dobutamine + NA + dopamine + adrenaline
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45
Q

What type of beta adrenergic drug is adrenaline + isoprenaline?

A

They are non-selective beta 1 + 2 agonists

  • cause tachycardia
  • isoprenaline increases rate & force of heart causing vasodilation = fall in diastolic
46
Q

What are beta 2 receptors used for?

A
  • responsible for smooth muscle relaxation of bronchioles, bronchus, uterine
  • Inhibits GI smooth muscle contraction
  • stabilises mast cells, preventing release of inflammatory mediators
  • have a higher affinity for adrenaline than NA

Beta-2 adrenoceptor agonists E.g. salbutamol, albuterol + terbutaline

Resistant to MAO

47
Q

What are alpha 1 agonists used for?

A
  • Postsynaptic
  • Receptors are found on blood vessels. NA is most potent at Alpha 1 receptors
  • E.g. phenylephrine stimulates alpha 1 receptors - used in hypotension + circulatory shock
  • vascoconstriction of blood vessels of skin, kidney + brain not GI tract
  • increase in BP
  • contraction of smooth muscle of ureters, mydiarisis (pupil dilation)
  • glucose metabolism
48
Q

What are alpha 2 agonists used for?

A
  • Presynaptic
  • they occur at NA nerve terminals
  • activation causes fall in cAMP which closes Ca2+ channels & stops further NT release
  • Centrally acting hypotensive drugs
    e. g. clonidine (used to decrease BP) + methyldopa
  • inhibit insulin release
  • stimulate glucagon release
  • Contraction of anal spinchter
  • inhibits release of NA + ACh
49
Q

Define Eupnea.

A

Normal breathing

50
Q

Define orthopnea

A

SOB when lying down.

51
Q

What are alpha-adrenoceptor antagonists used for?

A
  • vasodilation & drop in BP
  • increase urine flow by relaxing smooth muscle in the glands

E.g. prazosin, doxazosin (alpha 1 selective antagonist), phentolamine (non-selective)

Uses;

  • hypertension e.g. doxazosin (causes vasodilation + fall in arterial pressure
  • tumours of adrenal medulla e.g. phenoxybenzamine (stops large bolus of adrenaline release during surgery of removal of tumour)
  • urinary retention e.g. tamsulosin
52
Q

What are the effects of glucocorticoids?

A 
-reduces inflammatory and immunological response 
☹️can lead to increased susceptibility to infection, natural indicators of infection are inhibited-may progress unrecognised
-increases gluconeogenesis
☹️can lead to diabetes 
-increases protein catabolism
☹️can lead to muscle waisting and growth suspension in children
-increases bone catabolism 
☹️can lead to osteoporosis 
-mood
☹️can lead to psychosis
 -Increases gastric acid and pepsin
☹️ can lead to peptic ulceration
53
Q

What are the effects of mineralocorticoids?

A
  • increase Na+ reabsorbtion
  • increase K+/H+ excretion

This can lead to Na+ & H20 retention, hypokalaemia, hypertension and muscle weakness

54
Q

What stage of COPD requires GCS?

A

3rd stage

55
Q

Types of GCS?

A
  • hydrocortisone (used orally for replacement therapy and IV in shock & status asthmaticus)
  • pednisolone (orally in inflammatory and allergic diseases)
  • betamethasone and dexamethasone
  • beclometasone
  • triamcinolone (severe asthma)
56
Q

What are leukotriene inhibitors?

A

They are anti inflammatory drugs that interfere with the inflammatory actions of leukotrienes (WBCs)
E.g. zafirukast and montelukast (receptor antagonists)

Zileutron blocks the enzyme required for the formation of leukotrienes

57
Q

What are antiallergic drugs?

A

E.g. cromolyn and nedocromil

  • inhibit the antigen-antibody reaction on mast cells that trigger allergic reactions
  • Used to prevent symptoms of severe bronchial asthma, allergic rhinitis and exercise-induced bronchospasm
58
Q

What is an antigen?

A

An antigen is a protein which the body DOESN’T like that causes a reaction. It binds to receptors of mast cells forming an antigen-antibody complex =causes histamine to be released

59
Q

What do mucolytics do?

A

They break apart and liquefy thick respiratory secretions to facilitate easier removal.

E.g. acetycysteine, carbocysteine and bromhexine

Guaifensine is NOT a mucolytic

60
Q

Antihistamines inhibit H1 and H2 receptors. What’s the difference between 1st gen and 2nd gen?

A

1st generation e.g. chlorphenamine (piriton)

  • used for severe distress caused by itching
  • has anti musclarinic actions
  • Passes BBB -side effects = DROWSINESS

2nd generation e.g. loratadine (Claritin), cetirizine and fexofenadine (Allegra)

  • don’t have atropine like actions
  • DON’T cross BBB = cause less drowsiness
61
Q

What is the drug Nytol used for?

A

It’s an antihistamine, but it’s used for its side effects of sedation = sleeping tablet

62
Q

Where are mast cells predominantly found?

A

Lungs, GI tract and circulatory System

63
Q

What’s the half life of salbutamol and ipratropium?

A

Salbutamol- 3h

Ipratropium- 4h

64
Q

The pharmacological effects of antihistamines are result of…?

A

Blocking histamine (histamine antagonists)
And
Occupy ACh receptors to inhibit action of ACh (anticholinergic)

65
Q

What are the adverse effects of antihistamines?

A 
Drowsiness - use in caution if other depressants e.g. alcohol has been used
Mental confusion 
Sedation
Dry mouth -anticholinergic 
Anorexia
Epigastric distress 
Hypotension
Tachycardia
Urinary retention
66
Q

What are the cautions for antihistamines?

A 
Cardiovascular disease
Hypertension 
Increased intraocular pressure (glycoma)
Urinary retention 
Stenosing peptic ulcer
Sensitivity 
CNS depression
67
Q

The effect of ACh is EXCITATORY except..

A

In heart, which receives inhibitory cholinergic fibres from vagus, has inhibitory effects on rate & force of atrial contraction

68
Q

What’s the usage of musclarinic antagonists?

A
  • in anaesthesia- block vagal nerve = slowing heart & inhibit bronchial secretion
  • reduce intestinal spasm e.g. IBS
  • Parkinson’s Disease e.g. benzatropine
  • prevent motion sickness e.g. hyoscine
  • dilate pupils
  • Bronchodilator in asthma e.g. ipratropium
  • urinary incontinence e.g. solfenacin
69
Q

Where is ACh synthesised, stored and released

A

In cholinergic nerve terminals

70
Q

Why is cromoglicate not useful I’m an acute asthma attack

A

It is a prophylactic drug. Does have anti-inflammatory actions

71
Q

What is the main side effect for all drugs for a cough?

A

Drowsiness. Because antihistamines is the active ingredient in cough/cold preparations. Main side effect of antihistamines = drowsiness

72
Q

What are the different types of cough suppressants?

A
  • opiates
  • codeine phosphate (causes constipation + dependence)
  • morphine used in palliative care
  • OTC cough suppressants usually contain sedating antihistamines e.g. diphenhydramine
  • simple linctus -contains citric acid. Cheap + safe
73
Q

What are expectorants used for?

A

To aid expulsion of secretions when coughing

74
Q

Why shouldn’t mucolytics be used in pts with peptic ulcers?

A

Mucolytics interfere with the mucosal barrier in the stomach

75
Q

What are pulmonary surfactants used for?

A

Used in neonates to prevent respiratory distress syndrome. Immature lungs can’t produce surfactant. So pulmonary surfactants reduce surface tension in the alveoli + prevent lung from collapsing following expiration e.g. beractant given via ET tube

76
Q

Respiratory disorders can be divided into which 2 disorders?

A

Obstructive - cause narrowing of the airways e.g. asthma + bronchitis

Restrictive -where actual volume available in lungs for gas exchange is reduced e.g. pulmonary fibrosis

77
Q

What chemical causes airways to constrict?

A

ACh

Therefore ipratropium relaxes airways because it is a cholinergic antagonist

78
Q

What does it mean if someone is ‘atopic’?

A

They have a higher incidence of allergies due to increased levels of IgE antibodies in their blood.

79
Q

What are the characteristics of acute severe asthma?

A
  • peak expiratory flow (PEF) 33-50% of best normal
  • SOB, inability to complete sentence in one breath
  • RR >25
  • tachycardia >110
  • wheezing -may become absent if it becomes severe
80
Q

What are the characteristics of life-threatening asthma?

A
  • PEF <33% of best/predicted bets
  • SpO2 <92%
  • silent chest, cyanosis or feeble resp effort
  • bradycardia or hypotension
  • exhaustion, confusion or coma
81
Q

Salbutamol and salmeterol are both beta 2 agonists, what’s the difference?

A
  • Salbutamol is a short acting beta 2 agonist

- salmeterol is a long acting beta 2 agonist

82
Q

What is the direct action of salbutamol on the beta 2 receptor?

A
  • relaxes smooth muscle
  • inhibits mediator release from mast cells
  • may inhibit vagal tone + increase mucus clearance by an action on cilia
83
Q

Inhalation of beta 2 agonist may be in form of metered dose inhaler (MDI) how much of the drug stays in the lungs?

A

20% of inhaled dose is absorbed by body
10-25% stays in the lungs
The rest is swallowed 55-70%

84
Q

What are the side effects of beta 2 agonists?

A
  • tachycardia - reflex effect from increased peripheral vasodilation via beta 2 receptor
  • may cause hypokalemia - reduces potassium in blood esp if xanthines + steroids are used as well
  • dizziness & restlessness
85
Q

Evidence to suggest tolerance to salbutamol can occur, causing decline in number of beta 2 receptors in lungs, what can be taken to help this?

A

Steroids, because they inhibit beta receptor down-regulation

86
Q

What is the MOA of steroids in preventing asthma?

A
  • they are NOT bronchodilators
  • The REDUCE INFLAMMATION + allergic reactions
  • bind to glucocorticoid receptors in cytoplasm that regulate expression of multiple genes
  • inhibit leukotrienes & prostaglandins
  • inhibit downregulation of beta 2 receptor
87
Q

Name an oral + parental steroid used for asthma

A

Oral = prednisolone

Parental =hydrocortisone

87
Q

What are cromates used for?

A

They stabilise mast cells + prevents release of histamine. They are alternatives if steroids can’t be used.

87
Q

What are leukotrienes and what is their effect when activated?

A

They are released by eosinophils, basophils + mast cells. Activation of leukotriene receptors results in contraction + proliferation of smooth muscle, oedema, eosinophils migration + damage to mucous layer in the lung.

Leukotriene receptor antagonists have been developed for treatment of asthma -not very effective

88
Q

What’s the benefit of using a spacer?

A
  • allow greater evaporation of propellant + thus reduces particle size
  • reduce the velocity of aerosol
  • decrease deposition in throat + back of mouth (reduces incidence of thrush)
  • useful in coordination is poor
89
Q

When the SpO2 falls to 90% what is the PAO2?

A

8 kPa. Below this level cerebral hypoxia occurs

90
Q

Why does increased CO2 in body result in a fall in pH?

A

If the body increases its production of CO2, this increases production of carbonic acid, which dissociates to form hydrogen ions, resulting in a fall in pH (increased acidity) of cerebralspinal fluid.

The rate + depth of respiration is increased to get rid of excess CO2 via lungs = reduces carbonic acid + returns blood pH to normal.

91
Q

Why can respiratory acidosis occur in pts with respiratory disease?

A

In respiratory infection disease, there is difficulty in expiration + elimination of CO2. Therefore the number of hydrogen ions in blood increases = blood acidity increases. The hydrogen ions cannot be eliminated adequately as excess CO2 cannot be removed by increasing rate + depth of breathing.

92
Q

What detects low oxygen levels in the blood?

A

Low oxygen levels do not affect central chemoreceptors but are picked up by peripheral chemoreceptors in aortic arch + carotid sinuses. Oxygen level is very low before these are triggered. The response is to increase rate + depth of respiration.

93
Q

Why is giving to much oxygen to COPD pts bad?

A

Some pts with COPD have a gradual adaption to high concentrations of CO2, and are more reliant on low oxygen levels to stimulate breathing.

Administration of high oxygen concentrations may cause a rise in CO2 levels + increased acidosis by decreasing respiratory drive.

Uncontrolled oxygen can result in reduced respiration’s, CO2 necrosis and respiratory arrest

94
Q

What does the ANS regulation?

A
  • contraction + relaxation of smooth muscle
  • all exocrine + some endocrine glandular secretions
  • heart beat
  • some stages of metabolism
95
Q

Fibres that release NA are called….

A

Adrenergic

96
Q

ACh releasing fibres are called….

A

Cholinergic

97
Q

All preganglionic fibres are…

A

Cholinergic (release ACh)

98
Q

All postganglionic parasympathetic fibres are…

A

Cholinergic at their effectors

99
Q

Sympathetic postganglionic fibres release…

A

NA, but those innervation sweat glands of skin, some blood vessels + external genitalia release ACh.

100
Q

What % of adrenaline + NA does the adrenal medulla release?

A

85% adrenaline + 15% NA

101
Q

What are the anatomical differences between PNS + SNS?

A

PNS

  • fibres emerge from brain + sacral spinal cord
  • long Preganglionic fibres
  • short postganglionic fibres
  • ganglia in effector organs

SNS

  • fibres emerge from thoracolumbar region of SC
  • short preganglionic fibres
  • long postganglionic fibres
  • ganglia close to spinal cord
102
Q

How is NA broken down?

A
  • takes into cells + broken down by MAO in neural mitochondria
  • circulating NA destroyed by COMT
103
Q

What are the clinical effects of adrenaline?

A
  • increased cardiac output
  • rise systolic BP
  • vascoconstriction of skin
  • vasodilation in arteries in muscle
  • relaxation of smooth muscle
  • stabilisation of mast cell
  • rise in blood glucose

Side effects;
Anxiety, tremor, tachycardia, arrhythmias, hypertension, pulmonary oedema, N+V, sweating + dizziness

104
Q

What are beta-adrenoceptor antagonists used for?

A

E.g. propranolol, atenolol + bisoprolol (last 2 more selective at beta 1 only, less side effects)

Clinical effects

  • reduce the response of SNS = reduces force of cardiac contraction + slows HR
  • SA node automaticity reduced + AV node conduction time is pro,onged = bradycardia
  • bradycardia lengthens coronary artery perfusion time (during diastole) which increases oxygen supply to cardiac muscle (usueful for angina + MI)
  • antihypertensive effect
  • reduce LDL levels
105
Q

What are beta adrenergic antagonists used for?

A
  • Ischemic heart disease (reduces cardiac work + oxygen consumption)
  • heart failure (reduce hearts response to SNS)
  • hypertension
  • cardiac dysrhythmias
  • hyperthyroidism
  • anxiety
  • glaucoma (given as eye drops)
  • migraine (used in prophylaxis, affect cerebral blood vessels preventing vasodilation)
106
Q

What are the side effects of beta blockers?

A
  • bronchoconstriction
  • bradycardia, heart block or reduced cardiac output
  • depression
  • diabetes
  • weight gain
107
Q

What are the contraindications of beta blockers?

A
  • severe asthma - they can precipitate bronchospasm
  • severe depression
  • severe bradycardia, heart block, cardiogenic shock, untreated left Ventricular failure
108
Q

Name a MAOi

A

Phenelzine

Pharmacology (11 decks)

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