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MBCHB1 exam > phase 1 week 8 > Flashcards

phase 1 week 8 Flashcards

(60 cards)

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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
What does IgE do?
it forms a complex with mast cells | The allergen binds to this and causes the release of histamine, prostaglandins and leukotrienes
26
Describe intravenous administration
rapid onset by-passes liver permits titration drawbacks - increased adverse effects, requires IV access, infection, pain
27
Describe intramuscular admisnistration
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
Describe subcutaneous administration
``` absorption depending on blood flow constant and slow absorption prolonged effect by-passes lover drawbacks - pain, infection, delayed absorption in shock ```
29
Describe oral or rectal administration
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
What is bioavailability?
fraction of the administered drug dose that reaches the systemic circulation expressed as F
31
What factors may affect bioavailability?
drug factors - molecular weight, ionisation absorption - gastric pH / health of GI tract first pass metabolism (hepatic)
32
When does F=1?
for IV drugs
33
What is the volume of distribution?
apparent volume into which a known amount of drug must be dispersed to give the measured plasma concentration
34
What does volume of distribution depend on?
plasma protein and tissue binding molecular weight lipid solubility
35
What is volume distribution used to determine?
loading dose amount | elimination half-life, dosage interval
36
What is the loading dose?
target concentration X volume
37
What is clearance?
theoretical volume of plasma "cleared" of drug per unit time
38
What is half-life?
the time required for serum plasma concentrations to decrease by half
39
What is half life determined by?
clearance and volume of distribution | proportional to VD/CL
40
How many half-lives does it take to clear a drug?
4-5
41
When is a loading dose required?
drugs with a long half-life
42
What is meant by steady state?
the amount of drug administered is equal to the amount of drug eliminated within one dosing interval
43
How long does it take to reach steady state?
4-5 half lives
44
Describe type I hypersensitivity
immediate | IgE, mast cells - release of histamine and other inflammatory factors
45
What is type II hypersensitivity?
antibody-mediated
46
What is type III hypersensitivity?
immune complex -mediated
47
What is type IV hypersensitivity?
T cell - mediated
48
Describe transplant rejection
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
Describe public health
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
Describe the first wave of health improvement in the UK
1830-1900 classical public health interventions (water and sanitation), emerging civil and social order social reformers municipal authorites
51
Describe the second wave of health improvements in the UK
1890-1950 | science rationalism provides breakthroughs in many fields
52
Describe the third wave of health improvements in the UK
1940-1980 the welfare state and post-war consensus saw the emergence of the NHS, social security, social housing and universal education
53
Describe the forth wave of health improvements in the UK
1960-2000 effective health care interventions prolong life. Risk factors and lifestyle become a central concern in public health
54
Name some health concerns we face today
health inequalities obesity population growth and ageing demographic Human impacts of planet's life support system climate change
55
describe ion-channel linked receptors
also called transmitter-gate ion channels hydrophilic pores mediate passive transport show selectivity
56
Describe the mechanism of ion channel linked receptors
ligand (e.g. ACh) binds to multimeric receptor opens channel ions diffuse according to concentration gradient terminated by removal of ligand
57
Explain signal transduction via RTKs
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
Give an example of an RTK pathway
mitogen activated protein kinase (MAPK) - features ras, a monomeric g protein
59
Describe G proteins
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
Describe the mechanism of G protein coupled receptors
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

MBCHB1 exam (28 decks)

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