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mpharm year 3 sem 2 > week 6 > Flashcards

week 6 Flashcards

1
Q

who is Edward Jenson ?

A

man responsible for creating vaccination science- exposure to cow pox- leading to immunity from small pox

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2
Q

describe innate immunity (exam q) (5)

A
  • early phase of host response- first line
  • present in all individuals at all times
  • does not increase with repeated exposure
  • can discriminate between groups of pathogens
  • predates separation of animal and plant lineage
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3
Q

describe adaptive immunity (exam q) (5)

A
  • generated by specific lymphocytes (B and T cells)
  • can discriminate between individual pathogens
  • associated with ‘memory’
  • response gets better(more aggressive) and faster with each exposure
  • appears abruptly in evolution
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4
Q

where do all cellular elements of blood- including immune cells arise from?

A

pluripotent hematopoietic stem cells

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5
Q

do B cells and T cells come from lymphoid or myeloid lineage ?

A

lymphoid

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6
Q

do macrophages come from lymphoid or myeloid lineage ?

A

myeloid

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7
Q

do neutrophils and eosinophils come from lymphoid or myeloid lineage ?

A

myeloid

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8
Q

if the atomic barrier fails- what is the next line of defence?

A

complement/ antimicrobial proteins

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9
Q

if complement/ antimicrobial proteins fail, what is the next line of defence?

A

innate immune cells

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10
Q

if innate immune cells fail- what is the next line of defence?

A

adaptive immunity

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11
Q

give 2 examples of innate immune cells?

A

macrophages and natural killer cells

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12
Q

name one example of an antimicrobial protein

A

defensins

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13
Q

name 3 examples of an atomic barrier

A

skin
oral mucosa
respiratory epithelium
intestine

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14
Q

name 2 examples of cells involved in adaptive immunity

A

b cells
antibodies
T cells

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15
Q

name 3 sensor cells

A

macrophages
neutrophils
dendritic cells

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16
Q

what kind of cell is associated with: phagocytosis and activation of bactericidal mechanisms, antigen presentation?

A

macrophages

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17
Q

what kind of cell is associated with: killing of antibody coated parasites?

A

eosinophil

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18
Q

what kind of cell is associated with: antigen uptake in peripheral sites, antigen presentation?

A

dendritic cell

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19
Q

what kind of cell is associated with: promotion allergic responses and augmentation of anti-parasitic immunity?

A

basophil

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20
Q

what kind of cell is associated with: phagocytosis and activation of bactericidal mechanisms?

A

neutrophil

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21
Q

what kind of cell is associated with: release of granules containing histamine and active agents?

A

mast cell

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22
Q

which of innate and adaptive immunity is more specific?

A

adaptive

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23
Q

what is the different between b cells and macrophages in terms of receptors?

A

b cells have one highly specific receptor whereas macrophages have many receptors that cover a broad range

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24
Q

bacteria trigger macrophages to release what 2 things?

A

cytokines and chemokines

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25
Q

which region of the antibody will bind to the antigen?

A

variable

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26
Q

what region of the antibody can bind to macrophages?

A

constant region

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27
Q

why are epitopes important?

A

they are very shape dependent- if they are denatured or damaged and their shape is changed the antibody cannot bind to the antigen

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28
Q

what cell recognises the epitopes- even if they are buried inside an antigen

A

T cells

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29
Q

do T cells or antibodies recognise shape?

A

antibody

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30
Q

do T cells or antibodies recognise linear peptides?

A

T cells

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31
Q

how do dendritic cells initiate adaptive immune responses?

A

up-take antigen in the tissues and stimulate naive T lymphocyte activation, proliferation and differentiation

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32
Q

why are dendritic cells important in adaptive immunity?

A

specialised to ingest a wide range of pathogens and then express co-stimulatory molecules that support T cell proliferation and differentiation

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33
Q

name 4 non specific asthma stimuli

A

exercise
cold air
hyperventilation
chemical agents

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34
Q

name 2 different specific asthma stimuli

A

allergens
aspirin

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35
Q

name 5 characteristics of asthma (internally)

A
  • inflammation
  • hyper-responsiveness of smooth muscle to substances that cause contraction of smooth muscle
  • hypo-responsiveness of the smooth muscle to substances that relax smooth muscle
  • neuronal imbalance
  • hyperplasia (more of) and hypertrophy (bigger) airway smooth muscle
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36
Q

name 3 morphologic changes in bronchial asthma

A
  • lungs are over distended (due to over inflation)
  • small areas of atelectasis can be seen( dead tissue, coming away from lining- lack of oxygen)
  • occlusion of bronchi and bronchioles by thick tenacious mucous plug
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37
Q

name 2 cell types that are a marker of asthma when present in airway lumen

A

eosinophils and macrophages

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38
Q

name 6 structural (remodelling) changes in asthma

A
  • epithelial damage
  • mucosal oedema- more mucous
  • increased intraluminal secretions
  • basement membrane thickening
  • smooth muscle hypertrophy and hyperplasia
  • inflammation
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39
Q

describe how smooth muscle behaves differently in asthma

A

inflammation causes white blood cells present in lumen release inflammatory meditators which increase mediator and cytokine induced contraction
alteration in calcium control - causes changes in contraction and relaxation
proliferative response increases muscle mass and force of contraction
more contraction due to cytokines present in smooth muscle (hyper-responsive)

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40
Q

name 2 chemical changes as a result of asthma

A
  • higher amounts of Rho kinase - due to cytokine mediated gene induction -causes more sustained calcium contraction even when calcium returns to basal level
  • higher levels of M3 receptors- causes smooth muscle contraction and mucous secretion
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41
Q

name an example of an inflammatory mediator that can modulate adrenergic control

A

histamine

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42
Q

name 4 defects in cholinergic innervation associated with asthma

A
  • increased vagal tone
  • reflex bronchoconstriction
  • increased Ach released
  • increase post synaptic muscarinic receptor function
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43
Q

how do C fibres cause bronchoconstriction?

A

afferent nerves eg C fibres respond to histamine, bradykinin, prostaglandins etc to cause reflex bronchoconstriction

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44
Q

what does NANC stand for?

A

non adrenergic non cholinergic

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45
Q

give an example of a substance which causes NANC inhibition, does this cause relaxation or constriction?

A

nitric oxide
causes relaxation

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46
Q

give an 2 example of a substance which causes NANC excitation, does this cause relaxation or constriction?

A

substance P/ neurokinins
prostaglandins, bradykinin
causes constriction

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47
Q

describe the nature of seasonal rhinitis

A

symptomatic disorder - caused by exposure to allergens (pollen) via IgE mediated hypersensitivity reactions
Dendritic cells process allergens and present their peptides on the major histocompatibility complex (MHC)
Differentiation of naïve CD4 T cells to allergen specific Th2 cell- activated Th2 cells such as mast cells secrete histamine causing hey fever symptoms

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48
Q

name 3 treatment for allergic rhinitis

A

first line
- oral antihistamine
- intranasal antihistamine

second line
- leukotriene receptor antagonist

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49
Q

which sections of the skin are affected by eczema ?

A

epidermis and dermis

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50
Q

what is involved in the genetic predisposition to atopic dermatitis ?

A

a genetic predisposition to produce an exaggerated IgE mediated hypersensitivity reaction in response to harmless allergens

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51
Q

name 5 possible treatments for atopic dermatitis

A
  • emollient’s
  • topical corticosteroids
  • oral antibiotics therapy
  • antihistamine
  • light therapy (for chronic)
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52
Q

name 3 possible treatment for angio-oedema without airway involvement

A
  • trigger identification and avoidance (ie stop drug)
  • antihistamine
  • systemic corticosteroids
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53
Q

name 4 possible treatment for angio-oedema with airway involvement

A
  • trigger identification and avoidance
  • adrenaline and airway protection
  • antihistamine
  • IV systemic corticosteroids
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54
Q

name 3 treatments for mild psoriasis

A
  • topical corticosteroid
  • topical vitamin D analogue
  • topical coal tar
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55
Q

name 3 treatments for moderate- severe psoriasis

A
  • methotrexate
  • oral retinoid
  • ciclosporin
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56
Q

describe the underlying immunology for psoriasis

A

damaged keratinocytes during exposure to microbial or mechanical injury - activates macrophages and dermal dendritic cells which are antigen presenting cells (APC)
APC interact with T cells which produce a pro inflammatory cytokine

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57
Q

describe the mechanism behind a hypersensitive reaction

A

histamine is released when the trigger/ allergen causes B cells to activate and form plasma cells which then form IgE antibodies- which attach to mast cells
mast cells then activate- releasing granules containing histamine

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58
Q

state the 5 steps of an accuracy checking SOP

A

1- check patient details and bag label
2- check drug name, formulation, on Rx, product and label
3- check strength, dose, instructions on Rx, product and label
4- check quantity, expiry and PIL is inside
5- check pharmacy details, date dispensed, warning

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59
Q

what is the acceptable error rate in accuracy checking?

A

0.02%
2 in 10,000 items

60
Q

name 5 different cell types involved in asthma

A

mast cells
neutrophils
basophils
macrophages
eosinophils

61
Q

how are mast cells involved in asthma ?

A

these cells respond to allergen and IgE by releasing histamine and various interleukins like IL1

62
Q

how are macrophages involved in asthma?

A

these cells release prostanoids, cytokines and leukotrienes

63
Q

how are eosinophils involved in asthma

A

these cells release PAF, CSF which causes haematopoetic stem cells to differentiate into progenitor cells , GMSCF- which causes progenitor cells to differentiate into eosinophils

64
Q

why do NSAIDs not work in asthma?

A

NSAIDs reduce PGE2 and PGF2a in the lung
may also redirect activation of the leukotriene pathway which is contractile

65
Q

how do antihistamines not work in asthma?

A

even though mast cells product histamine- it is not so important in airway smooth muscle contraction in humans- works well in guinea pigs

66
Q

name 2 B2 adrenoceptor agonists

A

salbutamol
salmeterol

67
Q

which chemical functional group on salbutamol improves its selectivity ?

A

tertiary butyl group

68
Q

describe salbutamol and salmeterols MOA

A
  • inactivates MLCK (myosin light-chain kinase)
  • protein kinase A may inactivate ins (1,4,5) P3 receptors so that less calcium is released- inhibting contraction
  • calcium efflux pump (which reduces calcium levels) is increased by protein kinase A
  • this inactivates Raf-1 kinase which inhibits proliferation
69
Q

describe how salbutamol and salmeterol are different- how do they work differently?

A

salbutamol= short acting
salmeterol= long acting

salmeterol has lipophilic groups attached to it which interact with eco-sites on the receptor- this locks the ligand onto the receptor binding site- hence long acting

70
Q

is salbutamol or salmeterol more potent- how much more? why is this?

A

salmeterol - about 1000x more potent
binds for longer and more strongly at the receptor

71
Q

how do salbutamol and salmeterol use acetylcholine to affect smooth muscle ?

A

they inhibit its release- since it is an excitatory neurotransmitter it would constrict smooth muscle in the airway

72
Q

why is it useful that salbutamol and salmeterol can reduce vascular permeability ?

A

this stops there being too much fluid in the lungs which is particularly bad in asthmatic patients

73
Q

name the 3 mechanisms responsible for de- sensitisation

A
  • Phosphorylation of the occupied receptor by a specific receptor kinase, termed b-adrenoceptor kinase (b-ARK)
  • Internalisation of the receptor.(to take receptor into the cell, no receptor to activate anymore)
  • Phosphorylation of the occupied receptor by protein kinase A; e.g. negative feedback
74
Q

why is there less de sensitisation to salmeterol compared to salbutamol?

A

it is a partial agonist
therefore less phosphorylation of receptor and less internalisation of receptor

75
Q

name 3 issues with systemic delivery of salbutamol and salmeterol

A
  • increased blood flow- decrease in BP
  • increased glucose, fatty acids, ketones
  • increase in tremor in skeletal muscle
76
Q

explain how glucocorticoids work in asthma

A
  • dampen inflammatory responses
  • interacts with intracellular receptor- steroid binds to receptor- mediates transcription of anti inflammatory genes, transcribes new b2 adrenoceptors- negative effects on pro inflammatory genes
77
Q

describe what is meant by synergy between salbutamol and steroids in asthma treatment

A
  • work on 2 different pathways to do similar things- working together

ie steroids increase beta 2 receptor expression where salbutamol increases glucocorticoid receptor half life

why good- can use less of each drug- less side effects

78
Q

name a leukotriene inhibitor

A

montelukast

79
Q

name 3 things leukotrienes do that contributes to asthma symptoms

A

promote WBC in the area
causes constriction of airways
promotes inflammation

80
Q

name the pathway the leukotriene inhibitors act on

A

5 lipooxygenase pathway

81
Q

name 4 positive effects of theophylline in asthma

A
  • smooth muscle relaxation
  • inhibit anaphylactic release of mediators
  • suppress oedema
  • central stimulation of ventilation
82
Q

name 5 problems with using theophylline in asthma

A
  • side effects- anorexia, vomiting
  • non selective
  • dose needs to be low to avoid gI problems
  • CNS stimulation the maintenance dose is increased too quickly
  • serious toxicity can cause seizures
83
Q

why are antibodies a last resort treatment in asthma

A
  • very expensive
84
Q

how does antibody therapy work in asthma treatment ?

A

targets cytokine- gets rid of it

85
Q

what is spirometry used to diagnose?

A

airflow obstructions in patients with respiratory symptoms
also used to monitor progression, rehabilitation and treatment gains

86
Q

name 7 factors which can affect FEV1, FVC and/ or PEFR

A

gender
age
ace/ ethnicity
pollution exposure
smoking status
exercise
body weight

87
Q

what is the maximal amount of air exhaled steadily from full inspiration to maximal expiration described as?

A

slow vital capacity

88
Q

what is the volume of lungs form full inspiration to forced maximal expiration described as?

A

forced vital capacity

89
Q

what is the volume of air expelled in the first second of a forced expiration described as?

A

forced expiratory volume in one second

90
Q

why is FEV1 good in COPD (5 reasons)?

A
  • reproducible and objective
  • well defined reference ranges
  • quick and easy at all stages of disease
  • serial measurements can show disease progression
91
Q

why is peak flow not used in disease diagnosis?

A

cannot distinguish between obstruction and restriction of airway

92
Q

when is FER reduced?

A

in obstructive disease

93
Q

describe FVC in stage one COPD

A

mild- 80% or above FVC

94
Q

describe FVC in stage two COPD

A

moderate 50-79%

95
Q

describe FVC in stage three COPD

A

severe 30-49%

96
Q

describe FVC in stage four COPD

A

very severe below 30%

97
Q

when is reversibility testing used?

A

to distinguish between asthma and COPD

98
Q

what is reversibility testing?

A
  • baseline spirometry
  • bronchodilator (salbutamol) given
  • repeat spirometry test- increase of >400ml from baseline in FEV1 in suggestive of asthma
99
Q

productive cough? COPD? asthma? which is more likely ?

A

COPD
asthma tends to be dry cough

100
Q

which is more likely to cause sleep disturbances due to waking up breathless and wheezing, COPD or asthma?why?

A

asthma
COPD symptoms are constant- don’t change for time of day
asthma tends to get worse in the evening through to early morning- most asthma attacks are at 2-4 am

101
Q

how can methotrexate/ sulfasalazine affect COPD/asthma?

A

can cause interstitial pulmonary fibrosis- which is thickening of the lung tissue and thus losing elasticity- resulting in restriction of the pulmonary bed

102
Q

how do epithelial cells interfere with infection?

A
  • secrete mucous- interferes with adhesion of pathogens and results in expulsion resulting from beating of cilia
  • produce antimicrobial peptides such as B-defensins that damage bacterial cells membranes and surfactant proteins A and D that facilitate phagocytosis
103
Q

infectious agents induce inflammatory response by activating which kind of immunity?

A

innate

104
Q

epithelium penetration by infectious agents results in what ?

A

recognition of pathogen surface molecules by macrophages and subsequent phagocytosis

105
Q

activated macrophages secrete 2 chemicals, what are they and what do they do?

A

cytokines- affect behaviour of other cells
chemokine- attract other cells

therefore these 2 cell types initiate inflammation

106
Q

how do infectious agents induce adaptive immunity?

A

by activating DCs (dendritic cells)

107
Q

how do dendritic cells induce adaptive immunity?

A

DCs ingest pathogens in infected tissues
this is dependent on pathogen recognition receptors on macropinocytosis
DCs mature and migrate to peripheral lymphoid organs and present pathogen antigens to T cells which become activated and contribute to adaptive immunity

108
Q

epithelial cells can be activated directly by molecules such as - by what receptors?

A

molecules such as allergens
by receptors such as pattern recognition receptors or protease activated receptors

109
Q

how do allergenic proteases decrease barrier function?

A

by cleaving epithelial cell tight junction proteins

110
Q

name 2 cytokines produced by epithelial cells

A

IL-25
IL-33

111
Q

what can IL-25 and IL-33 cause?

A

cause migration and activation of DCs to induce T cell immune responses

112
Q

what are DCs necessary for inducing?

A

Th2 responses

113
Q

how do DCs promote Th2 differentiation?

A

DCs migrate regional lymph nodes and mature into cells that favour Th2 differentiation

114
Q

what does IL-4 promote ?

A

IgE production in B cells

115
Q

what does IL-5 promote?

A

drives eosinophil recruitment in lung tissue

116
Q

what does IL-13 promote?

A

causes bronchial hyper-reactivity

117
Q

how are ILC2s activated?

A

by IL-25 and IL-33

118
Q

what are ILC2s? when are they produced?

A

type of lymphoid cell
produced in response to injury or PAMPS

119
Q

ILCs secrete large amounts of what? and small amounts of what?

A

large- IL-5, IL-3
small- IL-4

120
Q

what do eosinophils synthesis? why do they do this?

A

mediators such as cytokines and leukotrienes- do this to amplify inflammatory response

121
Q

what does eosinophil peroxides do?

A

cause bronchial- hyper- reactivity and activation of DCs to drive Th2 polarisation

122
Q

how to mast cells contribute to bronchial hyper responsiveness?

A

by infiltrating the bronchial smooth muscle layer

123
Q

what triggers release of histamine (and other inflammatory mediators) granules from mast cells ?

A

multivalent antigen cross-links bound IgE antibody- causes release of granule contents

124
Q

name 1 biological effect of carboxypeptidases, try-taste or chymase

A

remodel connective tissue matrix

125
Q

name 3 biological effects of histamine and heparin

A

increase vascular permeability
cause smooth muscle contraction
anticoagulation
toxic to parasites

126
Q

name 1 biological effect of IL-4, IL-13 and IL-33 (cytokines)

A

stimulate and amplify Th2 cell response

127
Q

name 1 biological effect of IL-3, IL-5 and GM-CSF (cytokines)

A

promote eosinophil production and activation

128
Q

name 3 biological effects of TNF- alpha (cytokines)

A

promotes inflammation
stimulates cytokine production by many cell types
activates endothelium

129
Q

name 1 biological effect of CCL3 (chemokine)

A

attracts monocytes, macrophages and neutrophils

130
Q

name 5 biological effects of lipid mediators (prostaglandins (D2, E2) and leukotrienes (C4, D4, E4))

A

smooth muscle contraction
chemotaxis of eosinophils, basophils and Th2 cells
increase vascular permeability
stimulate mucous secretion
bronchoconstriction

131
Q

name 3 biological effects of platelet activating factor (lipid mediator)

A

attracts leukocytes
amplifies production of lipid mediators
activates neutrophils, eosinophils and platelets

132
Q

which characteristics are associated with neutrophil-prominent disease?

A

more severe
increase air remodelling
late onset
steroid resistance

133
Q

why is asthma difficult to diagnose?

A

it is diagnosed via symptoms but as it is reversible a patient may feel unwell and then in a few hours feel absolutely fine again

134
Q

how many times a week to use a SABA is too much?

A

asthma is uncontrolled if using it mote than twice a week

135
Q

inhaler steroid counselling (2)

A
  • ensure patient knows to take it even when they are feeling good- this is working
  • rinse mouth/ brush teeth after using to reduce chance of getting oral thrush
136
Q

why are Qvar and clenil not equal in dosing?

A

because of the difference in particle size, clenil is much bigger (10-15 microns) while Qvar is smaller (5 microns) - this is better for lung penetration

think how many letters in the word, smaller word, smaller particle etc

137
Q

why are steroid inhalers prescribed by brand?

A

different names of the same drug are not equal in dosing ie Qvar vs clenil- difference in particle size

138
Q

which kind of device is preferred for acute asthma ?

A

pMDI and spacer with titrated doses

139
Q

if patient has poorly controlled asthma - what do we do? (2)

A

try LABA first- if no benefit then stop
then try leukotriene

140
Q

step one of asthma plan

A

everyday asthma

preventer dose and counselling
reliever dose and counselling

141
Q

step two of asthma plan

A

when I feel worse
what symptoms to look for
waking at night
needing reliever more than3x per week
peak flow drops

  • increase preventer dose
142
Q

step three of asthma plan

A

asthma attack

  • Reliever isn’t helping or need it more than every 4 hours
  • Difficulty walking/ talking
  • Wheezing, tight chest
  • Blue inhaler
    *30-60 seconds between puffs- because, aerosol needs time – if don’t leave enough time -affects particle size and then lung penetration
  • Can use up to 10 puffs
     Then should call 999
     If managed to deal with the attack in house
  • See GP today
143
Q

what is MART ?

A

maintenance and reliever therapy- a combined inhaler

144
Q

caution with MART?

A

patient may take a high steroid dose
this should only be used a few times before seeking help

145
Q

steroids in pregnancy?

A

 Perfectly safe
 Explain to concerned patients that the amount of steroid passed to baby if tiny IF ANY- explain that If lucky 50% of dose will go into lungs
 The rest will stay in mouth or go to stomach
 Some absorbed in mouth, lungs, stomach- after this- distributed to liver where it is metabolised, then systemic circulation, then can get to baby via trans-placental distribution- ie VERY small dose can actually get to the baby
 If asthma is not well controlled during pregnancy- this poses a larger risk to baby via poor oxygen supply

146
Q

asthma in labour?

A

have salbutamol near by (reliever)
make sure healthcare team are aware

mpharm year 3 sem 2 (11 decks)

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