phase 1 week 8 Flashcards

1
Q

What is a cough?

A

An explosive expiration that provides a normal protective mechanism for clearing the tracheobronchial tree of secretions and foreign material

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2
Q

What may initiate the cough reflex?

A

excessive amounts of foreign matter or other causes of irritation

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3
Q

What forms the afferent limb of the cough reflex?

A

receptors within the sensory distribution of the trigeminal, glossopharyngeal, superior laryngeal and vagus nerves

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4
Q

What forms the efferent limb of the cough reflex?

A

the recurrent laryngeal nerve and the spinal nerve

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5
Q

Describe that caught reflex?

A

about 2.5 litres of air is inspired
epiglottis closes, vocal cords tightly shut to entrap the air within the lung
abdominal muscles contract forcefully, pushing against the diaphragm
internal intercostal muscles contract forcefully
pressure in lungs rises to 100mmHg or more
Markedly positive intrathoracic pressure causes narrowing of the trachea
vocal cords and epiglottis suddenly open widely
the large pressure difference between the airways and the atmosphere paired with tracheal narrowing produces rapid flow rates through the trachea

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6
Q

At what speed is air expelled from the lungs in a cough?

A

75-100mph

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7
Q

What are some factors that contribute to asthma?

A
environmental alleges
viral respiratory tract infections
exercise, hyperventilation 
gastro-oesophageal reflux disease
chronic sinusitis
aspirin or NSAID hypersensitivity
beta blockers
obesity
occupational exposure
emotional factors 
exposure to tobacco smoke
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8
Q

Describe the pathophysiology of asthma

A

It is complex and involves the following components;
airway inflammation
intermittent airflow obstruction
bronchial hypersensitivity

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9
Q

Describe airway inflammation

A

varying degrees of mononuclear cell and eosinophil infiltration, mucous hyper secretion, desquamation of epithelium, smooth muscle hyperplasia and airway remodelling are present

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10
Q

What are the main cells thought to be involved in airway inflammation?

A
mast cells
eosinophils
epithelial cells
macrophages
activated T lymphocytes
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11
Q

What are the main cytokines thought to be involved in airway inflammation?

A

IL-4, IL5, IL-6, IL-9, IL-13

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12
Q

What is the theory about TL1 and TL2 lymphocytes?

A

loss of balance between the cells types. In asthma TL2 is favoured - perhaps due to lack of infection exposure?

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13
Q

What causes airflow obstruction in asthma?

A

acute bronchoconstriciton
airway oedema
chronic mucous plug formation
airway remodelling

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14
Q

Describe the early asthmatic response

A

Response to aeroallergens

IgE dependent mediator release leads to acute bronchoconstriciton

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15
Q

Describe the late asthmatic response

A

airway oedema 6-24 hours after allergen exposure

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16
Q

What causes chronic mucous plug formation?

A

exudate of serum proteins and cell debris

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17
Q

what causes airway remodelling?

A

long-standing inflammation - may reduce the reversibility of the obstruction

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18
Q

What does airway obstruction cause?

A

Increased resistance to airflow and decreased expiratory flow rates
the changes lead to decreased ability to expel air and may result in hyperinflation

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19
Q

What does bronchial hyper responsiveness lead to?

A

bronchospasm and typical asthmatic symptoms such as

wheezing, shortness of breath and coughing

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20
Q

What can bronchospasm be a response to?

A
allergens
environmental irritants
viruses
cold air
exercise
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21
Q

What are the non-pharmacological management options for asthma?

A

smoking cessation
weight loss
breathing exercises

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22
Q

What are the pharmacological management options for asthma?

A

inhaled corticosteroids
long acting B2 agonist
short acting B2 agonist

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23
Q

How is complete control of asthma defined?

A
no daytime symptoms
no night time awakening due to asthma
no need for rescue medication
mo asthma attacks
no limitations on activity
normal lung function
minimal side effects from medication
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24
Q

What are the histological differences in asthma?

A

increase mucous production and increase goblet cells
increase eosinophils in mucous and cell tissue
thickened basement membrane
increased mast cells in lamina
increased neutrophils and T cells
smooth muscle hypertrophy

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25
Q

What does IgE do?

A

it forms a complex with mast cells

The allergen binds to this and causes the release of histamine, prostaglandins and leukotrienes

26
Q

Describe intravenous administration

A

rapid onset
by-passes liver
permits titration
drawbacks - increased adverse effects, requires IV access, infection, pain

27
Q

Describe intramuscular admisnistration

A

absorption depending on blood flow
by-passes liver
rapid onset and shorter in duration
drawbacks - neuromuscular damage, bleeding, pain, infection, delayed absorption in shock

28
Q

Describe subcutaneous administration

A
absorption depending on blood flow
constant and slow absorption
prolonged effect
by-passes lover
drawbacks - pain, infection, delayed absorption in shock
29
Q

Describe oral or rectal administration

A

convenient
safest
cheapest
slowest onset, prolonged by less potent action
drug passes through liver
Drawbacks - absorption rate can be highly variable, absorption influenced by stomach contents, gastric acid can interfere with absorption, uncooperative patients may not take them.

30
Q

What is bioavailability?

A

fraction of the administered drug dose that reaches the systemic circulation
expressed as F

31
Q

What factors may affect bioavailability?

A

drug factors - molecular weight, ionisation
absorption - gastric pH / health of GI tract
first pass metabolism (hepatic)

32
Q

When does F=1?

A

for IV drugs

33
Q

What is the volume of distribution?

A

apparent volume into which a known amount of drug must be dispersed to give the measured plasma concentration

34
Q

What does volume of distribution depend on?

A

plasma protein and tissue binding
molecular weight
lipid solubility

35
Q

What is volume distribution used to determine?

A

loading dose amount

elimination half-life, dosage interval

36
Q

What is the loading dose?

A

target concentration X volume

37
Q

What is clearance?

A

theoretical volume of plasma “cleared” of drug per unit time

38
Q

What is half-life?

A

the time required for serum plasma concentrations to decrease by half

39
Q

What is half life determined by?

A

clearance and volume of distribution

proportional to VD/CL

40
Q

How many half-lives does it take to clear a drug?

A

4-5

41
Q

When is a loading dose required?

A

drugs with a long half-life

42
Q

What is meant by steady state?

A

the amount of drug administered is equal to the amount of drug eliminated within one dosing interval

43
Q

How long does it take to reach steady state?

A

4-5 half lives

44
Q

Describe type I hypersensitivity

A

immediate

IgE, mast cells - release of histamine and other inflammatory factors

45
Q

What is type II hypersensitivity?

A

antibody-mediated

46
Q

What is type III hypersensitivity?

A

immune complex -mediated

47
Q

What is type IV hypersensitivity?

A

T cell - mediated

48
Q

Describe transplant rejection

A

T cells activated against donor transplantation antigens
stimulation in peripheral lymphoid tissues
Both CD4+ and CD8+ T cells
also macrophages, neutrophils, B cells, NK cells
Antigen production, compliment activation

49
Q

Describe public health

A

responds to societal health concerns
informed by a worldview prevailing at the time - science, ethics, aesthetic
led in different eras by different types of leaders and organisational forms

50
Q

Describe the first wave of health improvement in the UK

A

1830-1900
classical public health interventions (water and sanitation), emerging civil and social order
social reformers
municipal authorites

51
Q

Describe the second wave of health improvements in the UK

A

1890-1950

science rationalism provides breakthroughs in many fields

52
Q

Describe the third wave of health improvements in the UK

A

1940-1980
the welfare state and post-war consensus saw the emergence of the NHS, social security, social housing and universal education

53
Q

Describe the forth wave of health improvements in the UK

A

1960-2000
effective health care interventions prolong life.
Risk factors and lifestyle become a central concern in public health

54
Q

Name some health concerns we face today

A

health inequalities
obesity
population growth and ageing demographic
Human impacts of planet’s life support system
climate change

55
Q

describe ion-channel linked receptors

A

also called transmitter-gate ion channels
hydrophilic pores
mediate passive transport
show selectivity

56
Q

Describe the mechanism of ion channel linked receptors

A

ligand (e.g. ACh) binds to multimeric receptor
opens channel
ions diffuse according to concentration gradient
terminated by removal of ligand

57
Q

Explain signal transduction via RTKs

A

RTK monomers are single-pass transmembrane molecules
cytoplasmic domain has tyrosine kinase activity
extracellular ligand induces dimerisation of RTK monomers
Dimer undergoes autophosphorylation
creates phosphotyrosine residues on cytoplasmic domain
“docking sites” for intracellular proteins - scaffolds and substrates
Simultaneous activation of downstream pathways
RTK signalling often culminates in activation of enzyme or transcription factor

58
Q

Give an example of an RTK pathway

A

mitogen activated protein kinase (MAPK) - features ras, a monomeric g protein

59
Q

Describe G proteins

A

can bind to GTP
G proteins are GTPases- can hydrolyse GTP to GDP
G proteins may be monomeric or trimeric
Ras is a monomeric G proteins (in RTK pathway)
For G protein receptor coupled signalling must be trimeric G proteins

60
Q

Describe the mechanism of G protein coupled receptors

A

also called serpentine receptors
no intrinsic enzymatic activity
binding of ligand causes the receptor to undergo a conformational change
This lets a G protein bind to it
The binding of the receptor to the G protein phosphorylates the bound GDP to GTP
Alpha subunit with bound GTP activates effector enzyme
G protein then hydrolyses GTP back to GDP and protein is no longer needed so diffuses away