Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MPharm2 SL22107 > Pharmacology and Therapeutics > Flashcards

Pharmacology and Therapeutics Flashcards

1
Q

Which bacteria causes tuberculosis?

A

Mycobacterium tuberculosis

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

What are the survival rates for untreated TB?

A

untreated TB = 50%
untreated + HIV+ = ~0%

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

What are the 2 key properties of Mycobacterium tb.?

A
  • slow growing, doubling time is 15-24 hrs
  • acid fast bacteria
    • cell wall rich in lipids = thick waxy lipidic cell wall
    • very hydrophobic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 4 stages of TB?

A

Stage 1: exposure
- bacilli inhaled and settle in alveoli

Stage 2
- mild symptoms may appear
- a 3-4 week repeated cycle of bacteria multiplying in macrophages

Stage 3
- symptoms appear, cell-mediated response initiated
- collagen fibres formed around infected sites and granulomas form

Stage 4 - active TB
- bacteria multiply, granuloma bursts causing uncontrolled lysis
- enzymes released, destroy local tissue, cause lesions

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

What are the 3 outcomes of stage 3 TB?

A

45% - infection is cleared
45% - infection becomes latent
10% - progressive infection

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

What are the 5 symptoms of TB?

A
  • persistant and worsening productive cough
  • fever/chills
  • weight loss
  • fatigue
  • advanced TB - coughing up blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 3 ways that active TB diagnosed?

A
  • clinical examination
    • chest x-ray
      • white lesions
  • sputum test
    • ziehl-neelson stain
      • unlikely to see in early stage
      • cultures take 6 weeks
  • molecular assays
    • PCR
      • rapid (<2hrs)
      • sensitive
      • can detect resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 2 ways that latent TB is diagnosed?

A
  • Mantoux test
    • tuberculin skin test injected sc in forearm
    • positive test in development of a lesion >10mm in diameter
  • molecular test
    • interferon-gamma release assay
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the regulations surrounding TB screening?

A
  • compulsory on entry to UK if from a TB common country if staying for 6 months+
  • required for obtaining a visa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the immunisation procedure for TB?

A
  • BCG vaccination currently given to at risk babies, children and young adults
  • Used to be given to school children, stopped in 2005
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the first line treatment for TB?

A

RIPE
- Rifampicin
- Isoniazid
- Pyrazinamide
- Ethambutol

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

What are the 3 ways that Rifampicin works?

A
  • targets mRNA production
  • inhibits RNA polymerase
  • bactericidal to all metabolising cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 4 side effects of rifampicin?

A
  • liver damage
  • hypersensitivity
  • reduces activity of other drugs
  • red body fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does Isoniazid work?

A

Targets synthesis of mycolic acid, bactericidal to active bacilli, bacteristatic to slow-growing bacilli

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

What are the 4 side effects of Isoniazid?

A
  • hypersensitivity
  • peripheral neuropathy
  • liver toxicity
  • decreased efficacy of BC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does Pyrazinamide work?

A

Bactericidal to dormant bacilli, mechanism unclear. Pro drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 side effects of Pyrazinamide?

A
  • joint pain
  • liver damage
  • hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does Ethambutol work?

A
  • Increases permeability by affecting synthesis of arabinogalactan incell wall
  • Bacteriostatic to actively growing bacilli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 2 side effects of Ethambutol?

A
  • optic neuritis
  • joint pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the PK stats for RIPE drugs?

A
  • all orally absorbed and well distributed
  • all metabolised in liver and excreted by kidneys
  • however E is 50 % unchanged in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the sites of action for the RIPE drugs?

A

R - RNA polymerase
I - cell wall formation
P - ?
E - cell wall formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 2 ways to treat latent TB?

A
  • Isoniazid (6 months) or
  • Rifampicin + Isoniazid (3 months)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the 2 groups of second line anti-TB drugs?

A

Group A
- Levofloxacin
- Moxifloxacin

Group B
- Cycloserine
- Terizidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the two ways that MDR TB is treated?

A

Group A
- moxifloxacin
- linezolid

Group C
- pretomanid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 3 pillars of the End TB strategy?

A
  1. Integrated patient centred care + prevention
  2. Bold policies + support systems
  3. Intensified search + innovation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the autonomic nervous system?

A

The involuntary nervous system made up of sympathetic and parasympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the two neuron system?

A

pre-ganglionic system - cell body in CNS
post-ganglionic - cell body in autonoic ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the autonomic ganglion?

A
  • Interface between pre and post ganglionic neurones
  • ACh is primary transmitter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pre-synaptic fibres release…

A

ACh, which acts on nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Post-synaptic sympathetic fibres release…

A

Noradrenaline, which acts on adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Post-synaptic parasympathetic fibres release…

A

ACh, which acts on muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is ACh made of?

A

Choline and acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the ACh cycle of metabolism and synthesis?

A
  • In the synapse, ACh is rapidly broken down by acetylecholinesterases
  • Choline is transported back into the axon terminal and used to make more ACh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is sympathetic innervation of the airways?

A
  • most post-synaptic sympathetic fibres release NA, acting on adrenoceptors
  • NA is synthesised, stored and released from sympathetic nerves
  • very sparse sympathetic innervation of airways
  • sympathetic control via circulating adrenaline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the functions of adrenoceptors?

A

1 constrict most smooth muscle
except in GI tract where it relaxes

2 presynaptic inhibition of neurotransmitter release
sympathetic and parasympathetic neurones

β1 increases heart rate and force of constriction

β2 dilates/relaxes smooth muscle

β3 thermogenesis in skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is asthma?

A

A chronic inflammatory disorder of the airways
usually associated with
- variable airflow obstruction
- increase in airway response to a variety of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the two ways of testing lung function?

A

PEFR - peak expiratory flow rate
FEV1 - forced expiratory volume in 1 second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 4 mechanisms of hyperreactiveness in Asthma?

A
  1. increased smooth mucle contractility
  2. increased excitatory nerve activity
  3. decreased bronchodilator activity
  4. inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is Ipratropium?

A

A SAMA
- quaternary ammonium compound
- poorly absorbed
- lack of CNS effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the two bronchodilators used regularly in Asthma?

A
  • b-adrenoceptor agonists
  • phosphodiesterase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the excitatory chemicals?

A

ACh (M3 receptors)
eNANC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the inhibitory chemicals?

A
  • adrenaline
  • iNANC
  • NO
  • ACh (M2 receptors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the difference between intrinsic and extrinsic asthma?

A

Intrinsic
- non-atopic
- middle aged
- hyperresponsive
- severe airflow limit

extrinsic
- atopic (allergic)
- young onset
- hyperresponsive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the 3 ways that allergies can develop?

A
  • genetics
  • allergenic potential
    • physiochemical characteristics
    • ‘dosing regimen’
  • allergic disease associated with an increase in the Th2:Th1 ratio
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are Th1 cytokines?

A

Interferon-gamma
IL-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are Th2 cytokines?

A

IL-4 and IL-13
IL-5
IL-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What 4 factors increase your Th1?

A
  • older siblings
  • exposure at daycare
  • TB, measles, Hep A
  • rural environment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What factors increase your Th2?

A
  • widespread antibiotic use
  • western lifestyle
  • diet
  • sensitisation to dust mites etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is IgE?

A
  • relatively rare immunoglobulinin plasma
  • ‘erythmatous’ antibody
  • Fc region binds with high affinity to FcεR1on mast cell surface causes degranulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 4 mast cell granule products?

A
  • histamine
  • TNF and other cytokines
  • proteases
  • heparins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the 2 membrane-derived lipid mediators of inflammation?

A
  • leukotrienes
  • prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the role of eosinophils in allergy?

A
  • normally less than 1% of blood cells - rises to 5% in allergics
  • late phase response
  • IL-5 + chemokine induced migration
  • release basic proteins + ROS
  • produces cytokines, leukotrienes + prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How can H1 receptor antagonists be used in allergy?

A
  • chlorpheniramine, astemizole, cetrizine
    • effective in rhinitis, urticaria
  • little use for asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are chromones?

A
  • disodium cromoglycate, nedocromil
  • mast cell stabilisers - inhibit mediator release from lung mast cell
  • effective in about half patients
    • mostly early + late phase
    • antigen, irritant and exercis related
  • prolonged prophylaxis required
  • well tolerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is Omalizumab?

A

anti-IgE antibody
- monoclonal antibody
- prevent IgE binding to mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is immunotherapy?

A
  • escalating dose antigen
  • licensed for allergy
  • expensive
  • grass and tree pollen extracts
  • bee and wasp venom
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are inflammatory mediators in asthma?

A

smooth muscle
- contraction
- growth

epithelium
- damage
- secretion

bronchial venules increased
- blood flow
- permeability
- leukocyte adhesion

Leukocyte chemotaxis and activation
- eosinophils, T-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How are glucocorticoids used in allergy?

A
  • budesonide, inhalation
  • prednisolone, oral
  • reduce inflammation, swelling + mucus production
  • act mainly via regulating gene transcription
    - inhibit cytokine transcription
    - inhibit inflammatory leukocyte migration
  • indirectly inhibit phospholipase activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are PDE inhibitors?

A
  • PDE IV in leukocytes
  • PDE inhibitors increase intracellular cAMP
    • inhibits. chemotaxis, granule release, respiratory burst
  • Roflumilast, PDE IV selective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do leukotrienes impact asthma?

A
  • LTC4 + LTD4
    • potent constrictor of airway smooth muscle
    • increase mucus production
  • LTB4
    • no direct bronchoconstrictor
    • chemotactic for leukocytes
  • leukotriene receptor antagonist (montelukast)
  • leukotriene synthesis inhibitor (zileu)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How does IL-4 and 13 affect asthma?

A

Production of IgE
Eosinophil adhesion and migration
Increase eotaxin
Increase adhesion molecule expression
Increase mucus secretion and influence remodelling
Dupilumab anti-IL-4 receptor antibody used in severe asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How are eosinophils andanti-IL-5mAbs used as asthma therapy?

A

High numbers of eosinophils in asthmatic lung
Eosinophil products damaging to epithelium
IL-5 promotes eosinophil production, survival andactivation
Anti-IL-5 and anti-IL-5 receptor antibodies:
Possible indication in severe steroid resistant asthma
Benralizumab, mepolizumab, reslizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the 4 main symptoms of asthma?

A
  • coughing, wheezing
  • chest tightness
  • shortness of breath
  • variable expiratory airflow limitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the 7 risk factors of asthma?

A
  • Personal or family history of atopic disease (eczema, allergic rhinitis, or allergic conjunctivitis)
  • Respiratory infections in infancy
  • Exposure (including prenatally) to tobacco smoke
  • Premature birth and associated low birth weight
  • Obesity
  • Social deprivation
  • Exposure to inhaled particulates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the 10 main triggers of asthma?

A
  1. Allergens
  2. Irritants
  3. Respiratory infections
  4. Exercise
  5. Stress
  6. Medications
  7. Occupational hazards
  8. Allergic reactions
  9. Gord
  10. Hormonal changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is asthma diagnosed?

A

History
- Presence of typical symptoms and variable airflow obstruction
- Personal/family history of asthma and/or other atopic conditions (eczema, dermatitis, allergic rhinitis)

Tests
- FeNO test of 40ppb ( or 35 in children)
- Spirometry - FEV1/FVC usually >70%
- FEV1 improvement of 12% or more + increased volume of ≥ 200mL in response to meds
- Variable peak expiratory flow readings – over 20% variability at least BD for 2-4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the 3 requirements to prepare for a FeNO test?

A
  • Avoid exertion and smoking > 1h
  • Do not eat nitrate-rich food (green leafy veg, beetroot) > 3h
  • Avoid hot drinks, caffeine and alcohol > 1h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the 3 limitations of FeNO?

A
  • Insufficient expiratory effort
  • Effect of steroids (OCS and ICS)
  • Allergic rhinitis/rhinovirus infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How should treatment be progressed according to NICE?

A
  • Low dose ICS
    • LTRA (montelukast)
    • LABA (+ MART) +/- LTRA
  • switch to mod dose ICS
  • switch to high dose ICS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the advice given by BTS/SIGN when escalating treatment?

A
  • SABA for all at diagnosis
  • always check adherance before making changes
  • LABA before increasing ICS
  • Use combination inhalers to ensure adherance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the 6 lifestyle messages for asthmatics?

A
  • Stop smoking
  • Inhaler technique
  • Monitoring
  • Pharmacotherapy
  • Lifestyle
  • Education
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How are asthma exacerbations assessed?

A

Triggers
* Type and duration of Sx
* Assess the severity of the exacerbation:
*
PEF (best of 3 recordings) to grade the severity of the attack against the person’s best or predicted value:
* Moderate: more than 50–75%
* Acute severe: 33–50%
* Life-threatening: < 33%
O2 sats in room air using pulse oximetry
FeNO (if available)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is difficult asthma?

A

Difficult asthma (BTS/SIGN) - persistent symptoms and/or frequent asthma attacks despite treatment with:
- high-dose ICS plus a LABA/LTRA or
- continuous or frequent use of oral steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is severe asthma?

A

Severe asthma - asthma that is uncontrolled despite adherence with optimized high-dose ICS-LABA treatment with correct inhaler technique and management of contributory factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

When are asthma biologics used?

A

Relatively safe in comparison to other biologics
- Tertiary care only
- Patients need to be adherent to max ICS therapy and still experience exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is COPD?

A
  • Group of lung conditions that cause breathing difficulties
  • Characterised by progressive air flow limitation that is not fully reversible
  • Associated with an abnormal inflammatory response of the lungs to noxious particles or gases – primarily cigarette smoke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the 2 main conditions associated with COPD?

A
  • Chronic bronchitis
    • Productive cough present over years
    • Excessive sputum production
  • Emphysema
    • Alveolar wall destruction
    • Irreversible enlargement of the terminal air spaces
78
Q

What are the 3 common causes of COPD?

A
  • pollution
  • occupational hazards
  • smoking
79
Q

What are the 3 key differences between asthma and COPD?

A

Asthma has variable flow, while COPD has no varaibility.
Asthma is related to hyperesponsiveness, COPD is not.
Asthmatics have esinophilic-rich sputum, while COPDers have neutrophil-rich sputum

80
Q

What are the 4 mechanisms of airflow reduction in COPD?

A
  • Occlusion of airway by mucus
  • Thickened airway wall
  • Inflammatory cell infiltrate
  • Peribronchial fibrosis
81
Q

How is mucus produced in airways?

A
  • Mucous glands and goblet cells
  • Mucus production controlled by neuronal input and inflammatory mediators
82
Q

What causes inflammation in COPD?

A
  • Leukocyte infiltration
    • macrophages and CD8+ T cells
    • neutrophils in infection
  • Leukocyte products
    • Elastase & other proteinases
    • Reactive oxidant species
    • Chemoattractants
      • IL-8, LTB4
      • Recruit further leukocytes
  • Increased cytokines
    • increases mucin secretion from epithelium in vitro
    • induces elastase production
  • Macrophages and neutrophils release
    • proteases
      • break down connective tissue
      • stimulate mucus hypersecretion
      • Proteases are normally balanced by inhibitors
    • Reactive oxidant species
      • Damage epithelium
      • Activate inflammatory genes
      • Further damage
  • Macrophages and epithelial cells also release fibroblast growth factors
    • TGFb and EGF
    • implicated in fibrosis and mucus secretion
  • Cytotoxic T cells (CD8+) also implicated in the inflammatory cascade.
83
Q

What are the consequences of inflammation?

A
  • Epithelial damage
    • Decrease ciliary cell function
    • Increase mucus secretion from goblet cells
    • Mucus cell hyperplasia – more cells
    • Increased bronchial permeability
    • Airway oedema and protein exudation
  • Stimulation of sensory nerves
    • Neurogenic inflammation
    • Cough
84
Q

What causes a cough in COPD?

A

Motor reflex in response to sensing chemicals, particulates and excessive airway mucus
Sensory nerves sensitised by inflammatory mediators

85
Q

Why don’t bronchodilators work in COPD?

A
  • Bronchoconstriction not major cause of airway obstruction so b2 agonists often limited effect
  • Muscarinic antagonists
    • ipratroprium bromide some improvement
    • tiotropium & aclidinium have pharmacokinetic advantages
86
Q

What are phosphodiesterase inhibitors?

A
  • PDE III & IV in airway smooth muscle
    • Inhibition leads to bronchodilation
  • PDE IV in leukocytes
    • PDE inhibitors increase intracellular cAMP
  • Theophylline (weak, non-selective)
  • Roflumilast PDE IV selective
87
Q

What are mucolytics?

A
  • Mucus hypersecretion associated with decline in FEV1 and hospitalisation
  • Therapy - mucolytics
    • N-acetyl cysteine, carbocisteine, acetylcisteine
      • Breaks disulphide bonds in mucin
      • Anti-oxidant activity
  • Muscarinic antagonists
    • Block parasympathetic stimulation of secretion
  • Experimental treatments:
    • Neurokinin antagonists
    • Agents inhibiting sensory fibre activation
    • Neutrophil elastase inhibitor - brensocatib
88
Q

What are the 4 ways that corticosteroids are used in COPD?

A
  • Reduce inflammation
  • Inhaled for acute exacerbations
  • Small benefit from inhaledsteroids for maintenance
  • Given in combination with muscarinic antagonists
89
Q

What is emphysema?

A
  • Destruction of alveolar walls
  • Permanent enlargement of airspace distal to the terminal bronchiole
  • Reduces surface area of lungs for gas exchange
90
Q

What are lung elastases?

A
  • Strongly implicated in emphysema
  • Derived from neutrophils and macrophages
    include cathepsins, proteinase 3 and gelatinase
  • Degrade elastin, basement membrane and connective tissue
  • Increased after smoking
  • Serpins (serine protease inhibitors) inactivated by oxidant stress
91
Q

What are protease inhibitors?

A
  • a1-antitrypsin augmentation therapy in patients with deficiency
  • Elastase inhibitors
92
Q

What are antioxidants?

A
  • Vitamins C and E
  • N-acetyl cysteine
  • Limited evidence for efficacy
93
Q

Why don’t anti-inflammatory glucocorticoids work in COPD?

A
  • Oxidative stress results in decreased steroid sensitivity
    • Impaired glucocorticoid receptor function?
  • Neutrophil apoptosis inhibited by glucocorticoids
    • Compare with asthma – eosinophil apoptosis promoted by glucocorticoids
94
Q

What is histone acetyltransferase?

A
  • unpacks histones and allows RNA polymerase binding to DNA
  • Increased binding of transcription factors (NFkB, AP-1, CREB)
  • Increased inflammatory gene expression
95
Q

What is histone deacetylase?

A
  • Wraps DNA tightly in the histone
  • Decreases transcription factor binding
  • Suppression of inflammatory gene expression
96
Q

What are the 5 effects of glucocorticoids in COPD?

A
  • glucocorticoidsbind to glucocorticoid receptors
  • inhibits HAT and represses gene expression
  • cigarette smoke decreases glucocorticoid receptor binding
  • increases the activity of HAT
  • decreases the effect of HDAC
97
Q

How is COPD diagnosed?

A

History: medical, family and social
- Physical examination
- Assessment tools and questionnaires
- Post-bronchodilator spirometry (mandatory)
- Other tests e.g., chest X-ray, (HR)CT, ECG, blood tests

98
Q

What is the role of spirometry in COPD?

A
  • Diagnosis
  • Assessment of airflow obstruction severity (for prognosis)
  • Follow-up assessment
  • Therapeutic decisions
  • Identification of rapid decline
99
Q

What are the 3 COPD assessment charts?

A

CAT
Modified MRC Dyspnoea Scale
GOLD

100
Q

What are the 5 steps of providing the smoking cessation service?

A

Ask - identify users
Advise - urge to quit
Assess - determine willingness
Assist - help patient however you can
Arrange - follow up visit

101
Q

What are 9 elements of pulmonary rehabilitation?

A
  • oxygen therapy
  • learning about disease
  • clearance technoques
  • management of posture
  • taking respiratory medications
  • breathing exercises
  • managment of airway
  • exercise sessions
  • nutrition management
102
Q

What is type 1 respiratory failure?

A

Type 1 (hypoxic) respiratory failure – inadequate provision of oxygen to the body, leading to hypoxaemia
* Pulmonary oedema, pneumonia, PE, pulmonary fibrosis

103
Q

What is type 2 respiratory failure?

A

Type 2 (hypercapnic) respiratory failure – insufficient removal of carbon dioxide from the body, leading to hypercapnia
* Chest-wall deformities (e.g., kypho-scoliosis) or trauma, respiratory muscle weakness, COPD, severe obesity

104
Q

What is non-invasive ventilation?

A

Acute use in ECOPD hospitalised with acute respiratory failure
* In stable patients with severe COPD with hypercapnic respiratory failure and obstructive sleep apnoea
* Improves ventilatory pressure leading to better gas exchange
* Reduces respiratory rate, work of breathing, severity of breathlessness and mortality

105
Q

Howw should oxygen be used for COPD patients?

A

Oxygen (and any other medical gas) is a medication and needs to be prescribed
- For critically ill patients high concentration O2 should be administered immediately
- O2 saturation should be checked by pulse oximetry in all breathless and acutely ill patients

106
Q

What 4 things must be considered when prescribing oxygen?

A
  • concentration
  • rate
  • device/route
  • target saturation level
107
Q

What is long-term oxygen therapy?

A

Increases survival in those with severe chronic resting arterial hypoxaemia
* No benefit if no chronic hypoxaemia
* Must NOT SMOKE (including e-cig)
* Used minimum 15 hours daily
* Risks: respiratory depression, falls from tripping over equipment, burns & fires

108
Q

How is COPD treated palliatively?

A
  • Discussions with patients and their families about their views on resuscitation, advance directives and other relevant arrangements
  • Opioids, oxygen and fans blowing air onto the face can relieve breathlessness
  • Nutritional supplementation should be considered to improve respiratory muscle strength and overall health status
  • Fatigue common – can be improved by PR, nutritional support, self- management education and mind-body interventions
109
Q

What is a COPD exacerbation?

A
  • An event characterised by dyspnoea and/or cough and sputum that worsen over < 14 days.
  • Often associated with increased local and systemic inflammation caused by airway infection, pollution or other insults to the lungs
  • > 80% managed w/o hospital admission
110
Q

How is exacerbated COPD treated?

A
  • SABA/SAMA initially and review and escalate
    maintenance Tx
  • OCS (5/7) can improve FEV1, oxygenation and shorten recovery time
  • Abx (5/7), when indicated, can shorten recovery time and reduce the risk of early relapse, treatment failure and hospitalisation duration
  • Methylxanthines NOT recommended
  • NIV – first mode of ventilation in acute respiratory
    failure
  • Up to 4-6 weeks to recover, some don’t reach the baseline function
  • Tx goal: minimise negative impact of current ECOPD and prevent subsequent events
111
Q

What are mineralocorticoids?

A

e.g. aldosterone
– affect water and electrolyte balance

112
Q

What are glucocorticoids?

A

e.g. hydrocortisone and corticosterone
- affect carbohydrate and protein metabolism
- anti inflammatory and immunosuppressive effects

113
Q

What are the metabolic side effects of glucocorticoids?

A

Osteoporosis - (dec – collagen synthesis, osteoblast func, Ca absorption by inhibition of vitD action ) (Parathyroid hormone then increases Ca resorption from bone)

Diabetogenic due to dec in glucose uptake and utilisation and inc in gluconeogenesis plus increased appetite – obesity

Mineralocortocoid effects –Na/ H2O retention, hypertension, oedema and CV events

114
Q

What is the MoA of glucocorticoids?

A

Glucocorticoids enter cells and bind to cytoplasmic receptors.

Complex translocates to the nucleus to act as transcription factor

Can bind to response elements and activate anti inflammatory gene transcription

Can bind and repress pro-inflammatory gene activation
(eg COX-2, PLA2)

Can interact and inhibit binding of other transcription factors
(AP-1 and NFkB)

115
Q

What are the inflammatory effects of glucocorticoids?

A
  • Inhibit both early and late stages of inflammatory response
  • Decrease vasodilation and extravasation
  • Inhibit cell activation- TH (inhibit IL-2 and clonal expansion)
  • Decrease production of inflammatory mediators (ROS, prostanoids and leukotrienes, complement and histamine)
  • Endogenously prevent ‘overshoot’ of immune response
116
Q

What are the disadvantages of corticosteroids?

A
  • Many unwanted side-effects associated with GC actions
    Generally associated with high doses, systemic long-term admin
  • Immunosuppression can increase risk of infections
  • Impaired leucocyte traffic can delay wound healing
  • Suppress HPA axis through feedback inhibition
117
Q

How do you assess someone for exacerbated asthma?

A
  • Ask about possibletrigger factors, such as a recent upper respiratory tract infection.
  • Ask about the type and duration of symptoms, what treatment has been started (if any), and whether treatment has improved symptoms.
  • Assess the severity of the exacerbation: signs of exhaustion and cyanosis, record the respiratory rate, pulse, and blood pressure.
  • Record the peak expiratory flow rate and use the best of three recordings to grade the severity of the attack on the basis of the person’s best or predicted value:
    Moderate: more than 50–75%.
    Acute severe: 33–50%.
    Life-threatening: <33%.
  • Measure a person’s oxygen saturation in room air using pulse oximetry
  • Ask about social hx
118
Q

What are the 4 complications associated with severe eczema?

A
  • Infection
    • Bacterial infection with Staphylococcus aureus, which may present as typical impetigo or as worsening of eczema with increased redness, oozing, and crusting
    • Risk of herpes simplex and fungal infections
  • Psychosocial
    • Distress, missed school days, self image, sleep disturbances
  • Erythroderma
    • Erythroderma (a generalised redness of the skin) is a severe skin condition that can result in complications such as dehydration, heart failure, infection, and death
  • Eye abnormalities
    • Irritation of the conjunctivia
119
Q

How is eczema diagnosed?

A

Take a history and examine the rash

Assess severity
Mild: areas of dry skin, infrequent itching
Moderate: areas of dry skin, frequent itching and redness
Severe: widespread areas of dry skin, incessant itching and redness
Infected: if eczema is weeping, crusted, or there are pustules with fever and malaise

Consider using validated tools to assess severity
- Visual analogue scales (0–10) of the individual’s assessment of severity, itch, and sleep loss over the last 3 days and nights
- Patient-Oriented Eczema Measure
- Ask about the effect of eczema on daily activities (school, work, and social life), sleep, and mood.

None: no impact on quality of life.
Mild: little impact on everyday activities, sleep, and psychosocial well-being.
Moderate: moderate impact on everyday activities and psychosocial well-being, and frequently disturbed sleep.
Severe: severe limitation of everyday activities and psychosocial functioning, and loss of sleep every night.

120
Q

How can you identify the triggers of someones eczema?

A
  • Diet: ask about itch or redness after certain foods (immediately or hours later), diarrhoea, vomiting, and poor weight gain
  • Consider asking the person to keep a food diary over 4–6 weeks.
  • Irritants: ask about changes in soaps, detergents, and clothing, especially in previously well controlled eczema.
  • Inhalants: ask about symptoms around pets and pollen,
121
Q

How is mild eczema treated?

A

Advice
- avoid scratching
- house dust mite
- irritants
- stress
- diet

Prescribe generous amounts of emollients (liberal and frequent use)
Step up and consider a mild corticosteroid cream or ointment (and for 48hrs after flare has been controlled)
- Regular corticosteroid use should not be needed

  • Review annually emollient use and symptom control
122
Q

How is moderate eczema treated?

A

Advice – avoid scratching, house dust mite, irritants, stress, diet

Prescribe generous amounts of emollients (liberal and frequent use)
Moderately potent topical corticosteroid (betamethasone valerate 0.025% or clobetasone butyrate 0.05%) and continued for 48hrs
For delicate areas of skin (face and flexures) consider starting with a mild potency topical corticosteroid (hydrocortisone 1%) and increase to a moderate potency corticosteroid if needed (maximum of 5days use)
Occlusive bandages or dry bandages might be considered
Topical antibiotics if infected (max 2 weeks) – fusidic acid or mupirocin ointment if small areas or oral flucloxacillin

If there is severe itch of urticaria, consider prescribing a one-month trial of a non-sedating antihistamine (such as cetirizine)
Avoid triggers
Frequent and liberal emollient use
Topical corticosteroids – for flare prone areas
Either
Step down approach
Intermittent treatment

Topical calcineurin inhibitors (tacrolimus and pimecrolimus) are a second-line option (prescribed by a specialist, including GPs with a specialist interest in dermatology)

Identifying a flare early is considered to be important, as early treatment can reduce the severity of the flare and allow for more conservative treatment measures (such as emollients alone and reduced use of topical corticosteroids)

123
Q

How is severe eczema treated?

A

Advice – avoid scratching, house dust mite, irritants, stress, diet

Prescribe intensive treatment until the flare is controlled
Prescribe a generous amount of emollients and advise frequent and liberal use
Prescribe a potent topical corticosteroid for inflamed areas (betamethasone valerate 0.1%)
For delicate areas of skin such as the face and flexures, use a moderate potency corticosteroid (betamethasone valerate 0.025%, clobetasone butyrate 0.05%). Aim for a maximum of 5 days use
If itching is severe and affecting sleep, consider prescribing a sedating antihistamine (such as chlorphenamine) for adults and children aged 6 months or over (maximum two-week course) or non sedating if only daytime itching
Occlusive dressings or dry bandages may be of benefit
If there is severe, extensive eczema causing psychological distress, consider prescribing a short course of oral corticosteroids (> 16 years) (30 mg prednisolone in the morning for 1 week should be sufficient
If there are signs of infection, consider prescribing an oral antibiotic

124
Q

What are Topical calcineurin inhibitors?

A

Immunomodulating drugs
Inhibit calcineurin production which is responsible for inflammation in the skin (causing redness and itching)
Calcineurin is responsible for activation of T-lymphocytes, hence initiation of immune inflammation
Can be applied topically due to their low MW, hence has the ability to penetrate the striatum corneum

Does not have the same problems with long term use as steroids, so useful for use on the face and flexures

125
Q

What is tacrolimus?

A

Tacrolimus may be considered to treat moderate or severe atopic eczema for adults, or children aged 2 years or older, if the maximum strength and potency of topical corticosteroid that is appropriate for the patient’s age and the area being treated has been adequately tried and hasn’t worked, where there is serious risk of important side effects from further use of topical corticosteroids (particularly permanent damage to the skin)

126
Q

What is Pimecrolimus?

A

Pimecrolimus may be considered to treat moderate atopic eczema on the face and neck for children aged between 2 and 16 years if the maximum strength and potency of topical corticosteroid that is appropriate for the patient’s age and the area being treated has been adequately tried and hasn’t worked, where there is serious risk of important side effects from further use of topical corticosteroids (particularly permanent damage to the skin)

127
Q

How is severe eczema on hands treated?

A

Alitretinoin is recommended, as a treatment option for adults with severe chronic hand eczema that has not responded to potent topical corticosteroids

Alitretinoin treatment should be stopped:
as soon as an adequate response (hands clear or almost clear) or
if the eczema remains severe at 12 weeks or
if an adequate response (hands clear or almost clear) has not been achieved by 24 weeks.
Alitretinoin is a first generation member of the retinoid family, which also includes isotretinoin and acitretin (all related to Vitamin A)

Orally administered, the exact mechanism of action for hand eczema is unknown

128
Q

What can trigger an episide of psoriasis?

A

Streptococcal infection — strongly associated with guttate psoriasis, especially if the throat is infected
Some drugs – lithium, NSAIDs, beta-blockers
Sunlight
Trauma
Stress
Alcohol
Smoking
Climate changes
Hormone changes
HIV/AIDs

129
Q

What are the complications associated with psoriasis?

A

Psychological and social
Physical
Erythrodermic psoriasis substantially affects the body’s ability to regulate temperature and also affects haemodynamics, intestinal absorption, and protein and water metabolism
Generalized pustular psoriasis can cause fever, malaise, tachycardia, weight loss, and hypothermia, and has a significant mortality rate
Less severe psoriasis can also cause physical discomfort, including itch

Pregnancy

130
Q

What is the lifestyle advice given for psoariasis?

A

Nature of psoriasis, treatment aims and fact it is a chronic relapsing remitting condition that might not be fully treatable
Reassurance it is not an infectious condition
Referral to support groups/websites
Lifestyle advice to reduce flares – think triggers!
Referral for mental health support if needed

Range of information leaflets available. See CKS for the links

131
Q

How is plaque psoriasis on the trunk and limbs treated?

A

An emollient to reduce scale and help with other symptoms including itch (always apply often and first)
Potent topical corticosteroid applied once daily (review after 4 weeks, no longer than 8 weeks without a break) plus a vitamin D analogue applied once daily (Calcitriol or tacalcitol)
If response is poor after 8 weeks, continue Vit D analogue twice daily alone for up to 12 weeks.

2nd or 3rd line options are via a specialist – phototherapy or systemic therapy

132
Q

How is scalp psoriasis treated?

A

Treat with a potent topical corticosteroid (applied once a day max of 8 weeks – 4 week break as needed)
For people who cannot use corticosteroids on their scalp or who have scalp psoriasis that has not responded, consider treatment with a vitamin D preparation alone (applied once a day) or in combination with a potent corticosteroid scalp application
Coal tar preparations might be considered if treatment failure still occurs

2nd or 3rd line options are via a specialist – phototherapy or systemic therapy

133
Q

How is facial/flexural/genital psoriasis treated?

A

An emollient and short-term mild or moderate topical corticosteroid preparation (applied once or twice daily) for up to 2 weeks, only being used for 1-2 weeks each month

4 week treatment break as needed between corticosteroid courses

Do not use potent or very potent corticosteroids on the face, flexures or genitals

2nd or 3rd line options are via a specialist – phototherapy or systemic therapy

134
Q

How is guttate psoriasis treated?

A

referral

135
Q

How is pustular psoriasis treated?

A

Generalized pustular psoriasis — refer for same-day specialist assessment and treatment
It is a medical emergency that requires urgent hospital referral
Pustular psoriasis localized to the hands or feet — refer to a dermatologist. This is often difficult to control and usually requires systemic treatment

136
Q

How is Erythrodermic psoriasis treated?

A

Must be seen immediately, associated with life-threatening complications

137
Q

How is nail psoriasis treated?

A

Keep their nails short
Avoid manicure of the cuticle — this may provoke infection
Avoid fake nails
If nail disease is mild and is not causing discomfort or distress, no treatment is required.
Nail varnish can be used to disguise pitting, but abrasive acetone removers should be avoided.
If severe, refer to a dermatologist.

138
Q

How are corticosteroid creams used for psoriasis?

A

Topical corticosteroids are associated with adverse effects, as well as rebound psoriasis on discontinuation
Risk of serious adverse effects is low if used correctly

Greater risk if treatments are used for long periods of time on large areas, or potent or very potent steroids used incorrectly

Maximum of 8 weeks treatment, with 4 week breaks between use

139
Q

How are vitamin D creams used for psoriasis?

A

Vitamin D preparations bind to vitamin D receptors, which inhibits keratinocyte proliferation and enhances keratinocyte differentiation
6-8 week treatment is needed for best results
Topical vitamin D preparations should be avoided in people with Calcium metabolism disorders (can cause hypercalcemia), severe liver and kidney disease
Max 100g per week for creams and 60ml scalp solution
Side effects include skin irritation and photosensitivity

140
Q

How is coal tar used for psoriasis?

A

Coal tar is a distillation product of coal and has anti-inflammatory and anti-scaling properties

Newer products tend to be easier to apply

Can be applied long term

Not used with broken, infected & inflamed skin, genitals, rectum, pregnancy

Caution with face, flexures, late pregnancy and breastfeeding

141
Q

How is dithranol used for psoriasis?

A

Dithranol is thought to prevent T-lymphocyte activation and normalize keratinocyte differentiation

Dithranol should not be used in people with acute or pustular psoriasis, or inflamed psoriasis or used dithranol on the face

Short contact essential (0.1 to 2% creams and 30-60 minute contact time) increased weekly till lesion is palpably flat (then discontinue)

If skins becomes inflamed during treatment stop, and restart at a lower % when settled

142
Q

How is UV light therapy used to treat psoriasis?

A

Ultraviolet light reduces inflammation in the skin, which is why it can be effective for psoriasis
Narrowband (311-313nm) UVB is often used to treat guttate or chronic plaque psoriasis

The other type of therapy is known as PUVA, and is a combination of the UVA part of the spectrum and psoralen
Might be used if UVB has not worked, or if hands or feet are affected

BAD offers support leaflets on this therapy

143
Q

How are psoralens used to treat psoriasis?

A

Are drugs activated by long wave UV light (320-400nm)

They interfere with DNA synthesis hence reduce epidermal cell turnover, enhancing the effect of irradiation
Not licensed so prescribed under a named-patient basis
Either taken orally 2hrs before UVA, or applied topically immediately before exposure
If taken orally sunglasses are needed and nausea is a common side effect

Exposure depends on patient initially and increased, normally twice weekly for up to six weeks. Unless severe and relapsing repeat treatments should be avoided

144
Q

How is methotrexate used to treat psoriasis?

A

Folic acid antagonist used for severe psoriasis affecting high impact sites, and when phototherapy has failed, is contraindicated or has relapsed within three months
Can cause bone marrow suppression and should be taken once weekly at low dose

145
Q

What are two types of smooth muscle in the eye?

A
  • Iris smooth muscle
    dilator + sphincter to regulate pupil size
  • Ciliary muscle
    changes refractive index of lens
146
Q

What is mydriasis?

A

Pupil dilation

147
Q

What is miosis?

A

Pupil constriction

148
Q

What does a muscarinic agonists do to the eye?

A

Pupil constriction

149
Q

What does a muscarinic antagonist do to the eye?

A

Pupil dilation

150
Q

How do mydriatics work in the eye?

A

block constrictor muscle
- leads to pupillary dilation

151
Q

How do cycloplegics work in the eye?

A

paralyse ciliary muscle
- block accommodation

152
Q

How are muscarinic antagonists used to treat eye conditions?

A
  • Ocular examination: tropicamide
  • Anterior uveitis – inflammation
  • Amblyopia (lazy eye): atropine
153
Q

What is glaucoma?

A

Is a group of eye diseases that damage the optic nerve
It is associated with high pressure within the eye.
Classify in: Primary, secondary, developmental.
Glaucoma in one eye/both eyes

154
Q

Which groups are at increased risk of glaucoma?

A
  • Older
  • High blood pressure
  • African-carribean ethnicity
  • Family history of glaucoma
  • Diabetes
155
Q

How is intraocular pressure formed?

A

By rate of formation and rate of drainage of Aqueous Humour
AH produced continuously by ciliary body epithelium
Maintains intraocular pressure
Provides nutrients to cornea, lens etc
Released into posterior chamber

156
Q

How does aqueous humor circulate?

A

AH produced by ciliary body
AH flows from the posterior chamber through the iris into the anterior chamber
Trabecular meshwork (90%)
Canal of Schlemm & into vein
Uveoscleral outflow (10%)

157
Q

What is the composition of AH?

A

Ultrafiltrationof plasma
Produces nearlyprotein-free liquid
The high level of lactate is due toanaerobicglycolysis
The high level ofascorbic acidprotects against UV-radiation that can cause the formation of free radicals

158
Q

What are the inhibitors of AH formation?

A

a1 agonists
- vasoconstrictors
- decreased blood supply to ciliary body
a2 agonists
decreased cAMP, directly inhibits AH formation, decreased NA release from sympathetic fibres

159
Q

What are the 4 ways to treat glaucoma?

A

Eye drops: The different drops fall into five main categories, which work in slightly different ways: Alpha agonist, Beta blockers, Carbonic anhydrase inhibitors, Cholinergic inhibitors and Prostaglandin analogues.
Laser: Laser treatment is used in glaucoma to decrease the amount of fluid in the eye
Trabeculectomy surgery: A trabeculectomy is an eye operation that improves drainage of fluid out of the eye. Our trabeculectomy page explains how it works, what the surgery involves and what to expect after surgery
Aqueous Shunt Implantation: An aqueous shunt is a device which drains aqueous humour out of the eye to a small blister

160
Q

What is closed angle glaucoma?

A

More common in East Asian & Inuit populations
Angle between iris and cornea narrowed
Blocks flow of aqueous humour from posterior to anterior chamber
Onset can be sudden and result in rapid irreversible damage

161
Q

What is open angle glaucoma?

A

Obstruction of drainage through trabecular meshwork and canal of Schlemm
Intra-ocular pressure rises

162
Q

What is age related macular degeneration?

A

Macula is an oval-shaped pigmented region of the retina essential for ‘sharp’ vision
High density of cones (photoreceptors)

163
Q

What are the signs and symptoms of AMD?

A

Blurry spots in center of vision
Blank or dark spots in center of vision
Difficulty reading
Loss of clear color vision
Objects appear distorted
Straight lines that appear crooked or wavy

164
Q

What is dry AMD?

A

Most patients
Slow insidious onset
No successful treatments

165
Q

What is wet AMD?

A

Rapid onset
Choroidal neovascularization (abnormal blood vessels underneath the macula)
Excessive growth of leaky blood vessels under retina
Stopped with photodynamic therapy (PDT):
Verteporfin i.v. followed by laser photoactivation (red laser)
Occlusion of leaky blood vessels
Blood vessel growth & leak stimulated by vascular endothelial cell growth factor (VEGF)
Anti-VEGF antibodies or VEGF receptor constructs arrest progression
Other VEGF binding molecules – pegaptanib

166
Q

What is dry eye?

A

Dry eye syndrome (keratoconjunctivitis sicca) occurs when there is a problem with the tear film that normally keeps the eye moist and lubricated
Caused by a lack of tear production or increased evaporation of the tears

More common in women (50%) than men

167
Q

What are the complications associated with dry eye?

A

conjunctivitis and keratitis

168
Q

What are the symptoms of dry eye?

A

Dryness, grittiness, or soreness in both eyes
Vision might be affected
Watering of the eyes, particularly when exposed to wind

169
Q

What are the 5 differential diagnoses?

A

Conjunctivitis
Sjogren’s syndrome
Filamentary keratitis
Infectious diseases
Corneal damage

170
Q

What are the lifestyle intervention treatments for dry eye?

A

Eyelid hygiene
Limiting the use of contact lenses
Stopping medication that exacerbates dry eyes
Using a humidifier to moisten ambient air
Stopping smoking
If using a computer for long periods, ensuring that the monitor is at or below eye level, avoiding staring at the screen, and taking frequent breaks

171
Q

What is the first-line treatment for mild-moderate dry eyes?

A

Hypromellose (30 minute intervals initially then reduce as symptoms improve)
Carbomer or polyvinyl alcohol (used less frequently but less well tolerated)

172
Q

How is severe dry eye treated?

A

Preservative free preparations should be used
Ocular ointment at night

If there are visible strands of mucus – specialist only
Consider prescribing acetylcysteine drops (mucolytic drug)

If there is inflammation – specialist only
Consider prescribing a topical steroid or topical ciclosporin

Punctal occlusion

173
Q

What are liposomal sprays?

A

The use of liposomal sprays results in a clinically and significant increase in lipid layer thickness and tear film stability following application

They mimic what happens naturally when lipids are secreted from the meibomian glands
The sprayed-on phospholipid liposomes reach the lid margins via the same effect and mix with the endogenous lipids to help repair the tear film lipid layer

174
Q

What are the benefits of liposomal sprays?

A

The key benefit is that liposomal sprays aim to specifically address the disrupted lipid layer in evaporative dry eye (rather than simply bathing the eye in a short lasting tear replacement)
Stabilise the outer lipid layer
Last for up to 4 hrs
Can be used by contact lenses wearers
Easy to use – dexterity
Long expiry date after opening

175
Q

What are the disadvantages of liposomal sprays?

A

Not mentioned in guidelines
Expensive
Not allowed on prescription

176
Q

What are the 5 ways to assess glaucoma?

A

Direct observation of optic nerve (ophthalmoscopy)
Visual field examination (perimetry)
Assessment of intraocular pressure (tonometry)
Determine if open or closed angle (gonioscopy)
Measure of thickness of cornea (pachymetry)

177
Q

What are the 3 strategies for managment?

A

Medical treatment
Laser treatment
Surgical treatment

178
Q

What are the 5 drugs used for medical management?

A

Prostaglandin analogues
Beta-blockers
Carbonic anhydrase inhibitors
Sympathomimetics
Miotics

179
Q

How do prostaglandin analogues work for glaucoma?

A

Increase uvoscleral outflow
Most effective of all management options
Efficacy; bimatoprost > travoprost > latanoprost
Side effects; latanoprost > travoprost > bimatoprost
Eye colour / eyelid change

180
Q

How do beta-blockers work for glaucoma?

A

Reduces aqueous humour production
Betaxolol; shown to be neuroprotective by increasing blood flow
Effects of systemic absorption seen
Interactions
Systemic beta-blockers, anaesthesia, verapamil
Side effects
Breathlessness, bradycardia, dry eyes, masking hypoglycaemia

181
Q

How do carbonic anhyrdase inhibitors work for glaucoma?

A

Decrease production of intraocular fluid
Increase perfusion to eye, neuro-protective for ocular nerve head
Dose differs in monotherapy versus combination
Cross-reactivity with sulphonamides
Weak diuretic effect
Contraindicated in renal failure (CrCl <30mL/min)

182
Q

How do sympathomimetics work for glaucoma?

A

Very effective at reducing intraocular pressure
Decrease aqueous humour production, increase outflow
Cautions
Severe cardiovascular disease, cerebral/coronary insufficiency
Contraindicated with MAOIs
Side effects; blurred vision, discomfort, headache, nausea, hyperaemia

183
Q

How do miotics work for glaucoma?

A

Pull iris away from trabecular meshwork; improve outflow
Generally less well-tolerated than other agents
Cautions due to parasympathomimetic effects
Peptic ulcer, cardiac disease, asthma, epilepsy, Parkinson’s disease, hyperthyroidism, urinary tract obstruction

184
Q

How is glaucoma surgically treated?

A

Surgery to improve aqueous humour outflow
Trabeculectomy/trabeculotomy– remove part of eye drainage tubes
Viscocanalostomy –remove part of the sclera
Deep sclerectomy – widen the drainage tubes in eye
Trabecular stent bypass –trabeculoplasty to meshwork
Laser iridotomy; creates holes in iris
Surgery to reduce aqueous humour production
Cyclodiode laser; destroys tissue in eye responsible for aqueous formation

185
Q

What are trabecular interventions for glaucoma?

A

Trabeculoplasty, laser; trabeculectomy, surgery
Small hole in eye to improve outflow of fluid
May be more cost effective in advanced disease
More effective at reducing IOP, no difference in change in vision or QOL at 24 months
First-line by NICE but some resistance

186
Q

What is pharmalogical augmentation in glaucoma?

A

Scarring during the healing process can cause the outflow channel to close and the operation to fail with a rise in pressure
Use antimetabolites to prevent scarring by inhibiting the multiplication of cells which produce scar tissue.
Intraoperative mitomycin-C or 5-fluorouracil

187
Q

How do you re-assess patients with glaucoma?

A

Assess compliance with existing drops regimen
Goldman tonometry for IOP
Reassess for visual field defects

188
Q

What are the practical considerations when treating glaucoma?

A

Poor compliance; device, elderly population, side effects (drug/preservative)
Travoprost electronic aid study
#Knowyourdrops campaign
Check eye drop installation technique

Combination therapies; different dosing regimen
Local formulary choices
Brand versus generic prescribing
Preservatives
Contact lenses

189
Q

How is closed angle glaucoma treated?

A

Diuretics; mannitol, acetazolamide IV/oral to increase drainage
Pilocarpine to induce miosis
PGAs, beta-blockers, sympathomimetics
Surgery; cataract replacement, peripheral iridotomy

190
Q

What is paediatric glaucoma?

A

Raised intraocular pressure > 21 mmHg
Genetic mutation of trabecular meshwork / anterior chamber angle
Surgical management often required
Topical beta-blockers first line
Carbonic anhydrase inhibitors if contraindicated
PGAs preferred if juvenile-onset, less effective in young children
Adrenergic agonists CI in under 2s
Consider licensing and practical administration issues
Timolol LA reduced frequency but unlicensed

MPharm2 SL22107 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions