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Resp Flashcards

1
Q

What does mucus in respiratory epithelium do

A

Prevent dehydration of the epithelium

Trapped particles from inspired air

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2
Q

What are the swell bodies, where are they located and what are their significance

A

They are a thin plexus of blood vessels under the epithelium in the nose
They warm and humidify inspired air
They easily burst an cause nose bleeds

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3
Q

Where do each of the nasal sinuses drain into

A

Ethmoid drains into the upper turbinate
Maxillary drains into the middle turbinate
Frontal drains into the anterior aspect of the roof of the nasal cavity
Sphenoid drains into the posterior aspect of the roof of the nasal cavity

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4
Q

What is the olfactory epithelium and where is located

A

It is adapted for detection of odours and located in below the cribiform plate in the roof of the nasal cavity
The unmyelinated

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5
Q

What do the serous glands of Bowman and where are they found

A

They are found deep to the olfactory epithelium

They produce watery secretions that act as solvent for odorous substance
They irrigate the surface of the epithelium and refresh the olfactory epithelium

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6
Q

What is the difference between cilia and stereocilia

A

Stereocilia are immobile

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7
Q

What is the epithelium of the vocal cords

A

Stratified squamous epithelium

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8
Q

What is the epithelium of the larynx

A

Pseudostratified ciliated columnar epithelium with goblet cells (respiratory epithelium)

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9
Q

How many rings of cartilage hold open the trachea

A

12 - 15 C shaped rings

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10
Q

Which muscles lies at the back of the C shaped rings of the trachea

A

Trachealis muscle - it is smooth muscle

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11
Q

What kind of lymph nodes are found in the bronchi and how do they differ from normal lymph nodes

A

Part of the MALT (mucosa associated lymph tissue)

Normal lymph nodes are in a discrete encapsulated collection of lymphoid tissue

MALT are less discrete, do not have a capsule and are in mucosa

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12
Q

Difference between histology of the bronchi and the bronchioles

A

Bronchi contain hyaline cartilage

Bronchioles have no cartilage but a thick band of smooth muscle

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13
Q

Give some characteristics of the terminal bronchioles

A

They end the conducting part of the airways
Have simple cuboidal epithelium
Have clara cells
Lack cilia

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14
Q

Give some characteristics of the respiratory epithelium

A

They have simple cuboidal epithelium (form an acinus)

Non- ciliated

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15
Q

Are the terminal bronchiole bigger than respiratory epithelium

A

The respiratory epithelium is bigger than the terminal bronchioles

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16
Q

What do the type 2 pnuemocytes do

A

They synthesise store and secrete surfactant over the lining of the air sacs and facilitate inflation of the air sacs during inspiration
surfactant reduces surface tension and prevents desication

They are also stem cells from which Type 1 pnuemocyte come from

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17
Q

Length of air-blood barrier

A

Usually between 0.2 to 0.6um (same as 200 to 600nm)

If it is more than 1.2um then diffusion is seriously impaired

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18
Q

Which type of collagen lies in the walls of the alveoli

A

Reticulin (collagen 3)

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19
Q

What happens to particle- carrying alveolar macrophages, particle- carrying fixed septal macrophages and macrophages with large indigestible matter

A

Particle-carrying alveolar macrophages - enter respiratory and terminal bronchioles and into the musco-cilliary escalator

Particle-carrying fixed septal macrophages - remain in interstitium of lungs and enter lymphatics

Macrophages with large indigestible - macrophages fuse together to form giant cells, might induce granuloma formation

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20
Q

Give the layers of the blood- air barrier

A

Type 1 pnuemocytes
Basement membrane
Capillary endothelium

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21
Q

Give the nerve supply to the frontal sinus

A

The ophthalmic branch of the trigeminal nerve

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22
Q

Give the structures lining the outline of the maxillary sinus

A

Roof - floor of the orbit
Apex - zygomatic process of the maxill
Base - lateral wall of the nose
Floor - alveolar process near the teeth

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23
Q

Give the nerve innervating the maxillary sinus

A

The maxillary branch of the trigeminal nerve

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24
Q

Where does the maxillary sinus drain into

A

Through the hiatus semilunaris into the middle meatus

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25
Q

What nerve innervates the ethmoid sinus

A

The ophthalmic and maxillary branch of the trigeminal nerve

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26
Q

What structures lie close to the sphenoid sinus

A

Medial to the cavernous sinus which contains the carotid artery, cranial nerve 3, 4, 5 and 6

Inferior to the optic canal, dura and pituitary gland

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27
Q

What nerve innervates the sphenoid sinus

A

The ophthalamic branch of the trigeminal nerve

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28
Q

Where does the sphenoid sinus empty into

A

The sphenoethmoidal recess which is lateral to the nasal septum

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29
Q

Where does the ethmoid sinus drain into

A

Through the semilunar hiatus into the middle meatus

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30
Q

What does the internal superior laryngeal nerve do

A

Supplies sensation to all muscles of the larynx

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31
Q

How would you distinguish pulmonary arteries from pulmonary veins histologically

A

Pulmonary arteries have longitudinal elastic fibres running along their walls

Pulmonary veins have clearly defined media

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32
Q

What is the vestibule of the larynx

A

The area between the true and false vocal cords

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33
Q

Premature babies often experience a deficiency of surfactant in their lungs and this is because cells that produce surfactant develop late in gestation (28 weeks). What is the name of the condition and what does it cause

A

Infantile respiratory distress syndrome
There is lack of surfactant to reduce surface tension which makes it easier to inflate alveoli so there is widespread collapse of the alveoli

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34
Q

What does the ring of smooth muscle of the bronchioles do? What is its innervation and what is the consequence of continuous stimulation

A

Contraction of the smooth muscle causes bronchoconstriction (reduces lumen of the diameter of the bronchiole)

It is innervated by autonomic nervous system
parasympathetic nerves cause bronchoconstriction
Sympathetic nerves causes bronchodilation (beta-2-adrenoreceptors)

Continued contraction would cause

  • reduced airflow
  • seen in anaphylaxis and asthma
  • causes breathlessness and a wheeze
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35
Q

What do the nasal sinuses do

A

Lower the weight of the skull
Add resonance to the voice
Humidify and warm inspired air
Lined by respiratory epithelium

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36
Q

Where can Reinkes space be found

A

In the vocal cords
It is stratified squamous epithelium encircling loose irregular fibrous tissue
Has almost no lymphatics
Lies superficial to the vocalis muscle

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37
Q

Order of airways

A 
Trachea
Main bronchi
Lobar bronchi
Segmental bronchi
Bronchioles
Terminal bronchioles (last of conducting airways)
Respiratory brnchioles
Alveolar duct
Alveolus
Alveolar sac
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38
Q

What is the purpose of clara cells

A

Oxidise inhaled toxins
Antiprotease function
Produce surfactant
Stem cell purpose

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39
Q

What does the interstitium of the alveoli contain

A

Collagen and elastin fibres
Fibroblasts
Macrophages
Pores of Kohn (holes in alveoli walls)

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40
Q

What is the purpose of the pores of Kohn and what is its significance

A

Holes in alveoli wall
Helps to equalise pressure between adjacent alveoli
Helps lungs to inflate evenly
Can allow infection to spread quickly

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41
Q

What is special about visceral pleura layers

A 
Layer of mesothelial cells
Fibrocollagenous  connective tissue 
- irregular external elastic layer
- interstitial fibrocollagenous layer
- irregular internal elastic layer
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42
Q

Where do the intercostal veins drain into

A

The azygous vein on the right side and the hemi-azygous veins on the left side

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43
Q

Which nerves and blood vessels supply the foregut, midgut and hingut

A

Foregut - great splanchnic nerves arising from T5 - T9 (Coeliac axis)
Midgut - lesser splanchnic nerves arising from T10 - T11 (Superior mesenteric artery)
Hindgut - least splanchnic nerves arising from T12 ( Inferior mesenteric artery)

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44
Q

Where can pain be felt in the foregut, midgut and hindgut

A

Foregut - epigastrium
Midgut - umbillicus
Hindgut - suprapubic area

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45
Q

Where do the left and right vagus nerve enter the diaphragm and with which structure

A

They enter the diaphragm at T10 with the oesophagus
The left vagus nerve is anterior to the oesophagus
The right vagus nerve is posterior to the oesophagus

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46
Q

Where does the thoracic duct drain into

A

Into the confluence of the left subclavian vein and the internal jugular vein on the left side of the neck

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47
Q

What is trans-oesophagheal echo (TOE) used for

A

A trans-oesophagheal probe can be put into the oesophagus which is posterior to the mitral valve and can be used to get good images of it (sits on the posterior aspect of the heart)

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48
Q

What can damage to the stellate ganglion (T1) cause

A 
Loss of sympathetic innervation to the face and eye
No face sweating (anihydrosis)
Drooping eyelid (ptosis)
Constricted eye pupil (miosis)
Eyes drawn in (enopthalmus)
This is known as horners syndrome
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49
Q

What structures drain into the azygous vein

A

The posterior and lateral chest wall

The posterior and lateral abdominal wall

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50
Q

What do the sympathetic nerves attach to the central nervous system

A

T1 - L2

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51
Q

Where does the nasolacrimal duct drain into

A

The inferior meatus

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52
Q

What gives motor innervation to the cricothyroid muscle

A

The external superior laryngeal nerve (branch of the vagus nerve)

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53
Q

What gives motor innveration to the muscle of the larynx except the cricothyroid muscle

A

The left and right recurrent laryngeal nerve

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54
Q

What gives sensory innervation to the muscles of the larynx

A

The internal superior laryngeal nerve

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55
Q

Where does the right recurrent laryngeal nerve loop

A

Under the right subclavian artery in the neck

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56
Q

What can blood gas measure

A

PaCO2
PaO2
pH
HCO3-

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57
Q

What is health psychology

A

Health psychology emphasises the role of psychological factors in the cause, progression and consequences of health and illness

Aims to put theory into practice by promoting health behaviours and preventing illness

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58
Q

Give the 3 categories of health behaviours

A

Health behaviour
Illness behaviour
Sick role behaviour

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59
Q

What does health behaviour consist of

A

It is aimed at preventing disease (e.g eating healthily)

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60
Q

What does illness behaviour consist of

A

Aimed at seeking remedy (e.g like going to the doctor)

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61
Q

What does the sick role behaviour consist of

A

Any activity aimed at getting well (e.g taking prescribed medications and resting)

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62
Q

Give some examples of health damaging and health impairing behaviour

A 
Smoking
Alcohol and substance abuse
Risky sexual behaviour
Medication compliance
Vaccinations
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63
Q

Give some examples of health promoting behaviour

A 
Healthy eating
Exercising
Attending health checks
Medication compliance
Vaccinations
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64
Q

Give some examples of modifiable risk factors

A 
Diet/ Excess weight (obesity)
Smoking
Alcohol intake
Lack of exercise
Sleep and stress
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65
Q

Give some examples of non-modifiable risks

A

Gender
Sex
Genetics/Family History

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66
Q

Give an example of a population level intervention

A

Health promotion - which is the process of enabling people to exert control over the determinants of health thereby improving health e.g

Health promotion campaigns like Change 4 Life, Stoptober, Movember, Everyone likes a drink but no one likes a drunk

Promoting screening and immunisations

  • cervical smear screening
  • MMR vaccine
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67
Q

Give an example of an individual level intervention

A

Patient centred approach - which give care responsive to individual needs

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68
Q

Give example of primary intervention at an individual’s behaviour, local community and population level using alcohol consumption

A

Individual’s behaviour - level of alcohol consumption and individual health outcomes

Local community - local alcohol sales, alcohol related crime and accident

Population level - national alcohol sales and consumption, national statistics on alcohol related crime and A&E events

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69
Q

What is unrealistic optimism

A

This is when individuals continue to engage in health damaging behaviour due to inaccurate perceptions of risk and susceptibility

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70
Q

Give factors that affect people’s perception of risk

A
  • Lack of personal experience with the problem
  • belief that the problem is preventable by personal action
  • belief that if it has not happened by now, it is unlikely to ever happen
  • belief that the problem is infrequent
Also 
Health beliefs
Situational rationality
Culture variability
Socioeconomic factors
Stress
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71
Q

Give some models and theories of behaviour change

A
  • Health belief model (HBM)
  • Theory of planned behaviour
  • Stages of change (transtheoretical) model
  • Motivational interviewing (MI)
  • Social marketing
  • Nudging (choice architecture)
  • Financial incentives
  • Social norms theory
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72
Q

Give the 4 aspects of the Health belief model

A

The individual will change if they believe;

  • they are susceptible to the condition (e.g heart disease)
  • it has serious consequences (e.g death)
  • taking action will reduce susceptibility (e.g stopping smoking)
  • the benefits of taking action outweigh the costs (e.g good health instead of heart failure)
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73
Q

Give the aspects of the theory of planned behaviour and give the 3 factors that determines intention

A
  • Proposes the best predictor of behaviour is ‘‘intention’’

3 factors that determine intention

  • a persons attitude to the behaviour = attitude
  • the perceived social pressure to undertake the behaviour = subjective norm
  • a persons appraisal of their ability to perform the behaviour = perceived behavioural control
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74
Q

Give examples of the 3 factors that affect the intention in the theory of planned behaviour model

A

Attitude = I do not think smoking is a good thing
Subjective Norm = most people who are important to me want me to give up smoking
Perceived behaviour control = I believe I have the ability to give up smoking

Behavioural intention - I intend to give up smoking

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75
Q

Explain the aspects the stages of change model (transtheoretical moel)

A

This models sees the individuals in discrete ordered stages rather than on a continuum

It proposes 5 stages of change;

Precontemplation (not ready yet)
Contemplation (thinking about it)
Preparation (30 days to get ready)
Action (3 to 6 months of doing it)
Maintenance (more than 6 months of the behaviour)
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76
Q

Give the 5 aspects of the transtheoretical model, the time required for it and examples with smoking

A

Precontemplation (not yet ready) - no intention of giving up smoking
Contemplation (thinking about it) - beginning to consider quitting smoking
Preparation (30 days to prepare) - getting ready to quit smoking
Action (3 to 6 months doing it) - engaging in giving up smoking now
Maintenance (more than 6 months dong it) - steady non-smoker

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77
Q

In the UK, how many people per year are affected by community acquired pneumonia and how many of these are admitted to hospital and die?

A

250000
33% are admitted to hospital
10% of those admitted to hospital die

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78
Q

Give some symptoms of acute respiratory distress syndrome?

A

Respiratory failure
Water and neutrophils fill the alveoli
Endothelial leak - mass of protein and fluid
Lungs - reduced compliance, increased shunting
Heart - hypoxia, pulmonary hypertension and reduced cardiac output

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79
Q

How are pathogens recognised in the body

A

Through pathogen recognition receptors (PRRs)

Like for signalling e.g Toll-like receptors (TLRs) and Nod-like receptors (NLRs)

Like for endocytic e.g Mannose receptors, Glucan receptors and Scavenger receptors

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80
Q

How is acute inflammation initiated

A

Epithelial cells produce hydrogen peroxide
Macrophages converge
They respond to pathogen associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs)

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81
Q

Give some example of Toll-like receptors and their uses

A

TLR2 recognises lipotechoic acid (LTA) in gram positive bacteria
TLR4 recognises lipopolysaccharide (LPS) in gram negative bacteria

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82
Q

Give the primary and secondary granules present in neutrophils

A

Primary - myeloperoxidase, elastase, cathpsins, defensins

Secondary - receptors, lysozyme, collagenase

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83
Q

Give the 6 functions of the neutrophil

A
  • identify the threat (opsonin on pathogen/host, host mediators, host adhesion molecules)
  • activation (signal transduction pathways including calcium, protein kinases, phospohlipases, G proteins)
  • adhesion (margination is caused by selectins, adhesion is caused by integrins)
  • migration/ chemotaxis (detecting a concentration gradient and moving along it)
  • phagocytosis (membrane invagination forming phagosome and fuses with lysosomes to form phagolysosome)
  • bacterial killing (lysosomal enzymes e.g cathepsins, elastase and reactive oxygen species) (reactive oxygen species created by NADPH oxidase)
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84
Q

What is physiological dead space

A

The area in the airways that do not contribute to ventilation

Anatomical (125) + alveoli (50) = 175m/s

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85
Q

Difference between ganglion location and neurone length of the parasympathetic and sympathetic nerves

A

Parasympathetic nerves have ganglion close to the target organ

  • pre-ganglionic (pre-synaptic) nerves are long
  • post-ganglionic (post-synaptic) nerves are short

Sympathetic nerves have ganglion close to the vertebrae (sympathetic chain)

  • pre-ganglionic (pre-synaptic) nerves are short
  • post-ganglionic (post-synaptic) nerves are long
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86
Q

What are the cranial parasympathetic nerves

A

1973

Nerve 10, 9, 7 and 3

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87
Q

How is smooth muscle tone in the airways regulated

A

Regulated by inflammation

Regulation by the autonomic nervous system

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88
Q

What is the dominant control of bronchoconstriction

A

The parasympathetic nervous system

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89
Q

How does bronchoconstriction occur

A

Vagus nerve (long pre-ganglionic) stimulation synapses on the parasympathetic ganglia in the airway wall
Short post-synaptic nerve fibres reach the smooth muscle and release acetylcholine (ACH)
Acetylcholine acts on the M3 muscarinic receptors in the smooth muscle of the airways
This causes airway smooth muscle constriction

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90
Q

What is the action of the drugs that inhibit the parasympathetic nervous system in excessive bronchoconstriction conditions like asthma

A

Anti-muscarinic and anti-cholinergic
They block the M3 receptors of the smooth muscle in the airways which then causes bronchodilation

Short acting muscarinic antagonists (SAMA) e.g ipratropium bromide (atrovent)
Long acting muscarinic antagonists (LAMA) e.g tiotropium, glycopyrrhonium

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91
Q

Which receptors does noradrenaline act on, in which nervous system and what do they cause

A

Alpha receptors - cause vasodilation
Beta receptors - cause vasoconstriction
Beta-2-receptors - causes bronchodilation (think beta-2-agonists encourage its action)

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92
Q

Instead of SAMAs and LAMAs, what drugs can be use instead to cause bronchodilation

A

Short acting beta agonists (SABAs) e.g Salbutamol

Long acting beta agonists (LAMAs) e.g formoterol and salmeterol

SABAs and LABAs prevent bronchoconstriction and relieve acute bronchoconstriction, they also reduce the rates of exacerbatios

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93
Q

What does the non-adrenergic non-cholinergic nervous system (NANC system) do in the airways

A

Nothing really

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94
Q

Give some chemical epithelial barriers (molecules) produced by respiratory epithelium

A

Anti-proteinases e.g SLPI, lysozyme and phospholipase A
Anti- fungal peptides e.g alpha-defensins
Anti- microbial pepties e.g beta-defensins
Surfactant A and D - they opsonise pathogens for enhanced phagocytosis

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95
Q

What is a cough

A

An expulsive reflex that protects the lungs and respiratory passages from foreign bodies

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96
Q

Causes of a cough

A

Irritants e.g smoke, fumes, dust
Diseased conditions e.g COPD and tumours
Infections e.g influenza

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97
Q

What is a sneeze

A

The involuntary expulsion of air containing irritants from the nose

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98
Q

Causes of a sneeze

A

Irritation of the nasal mucosa

Excess fluid in the airways

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99
Q

What is a pack year history and how is it calculated

A

It measures the smoking history of patients

20 cigarettes in a pack

To calculate

Number of years x number of packs per day smoked = pack years
2 years x 2 packs (40 cigarettes a day) = 4 pack years
1 year x 0.5 pack (10 cigarettes a day) = 0.5 pack years

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100
Q

What is global health

A

Health problems, issues and concerns that transcend national boundaries, may be influenced by circumstances or experiences in other countries and are best addressed by cooperative actions and solutions

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101
Q

Where was the greatest number of cases in ebola in 2014

A

Liberia

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102
Q

Where did the ebola outbreak start in 1976

A

In Democratic republic of congo

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103
Q

Where did the ebola outbreak start in 2014

A

In Guinea

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104
Q

What is the leading cause of death globally

A

Cardiovascular disease (heart disease)

Followed by cancer

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105
Q

Important risk factors for mortality and disability in poor countries

A

Underweight
Unsafe sex
Unsafe sanitation and drinking water

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106
Q

Important risk factors for mortality and disability in developed countries

A

Tobacco
High blood pressure
Alcohol
High cholesterol

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107
Q

Give some countries that demonstrate patterns of population change

A

Rapid growth e.g democratic republic of Congo
Slow growth e.g United States
Negative growth e.g Germany

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108
Q

What is the biggest global health challenge

A

Access to information

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109
Q

What are the Millennium Development Goals (MDGs)

A

The millennium development goals are the eight goal that were meant to be achieved by 2015 to address the world’s main development challenges

These include

1) Eradicate extreme poverty and hunger
2) Achieve Universal Primary education
3) Promote Gender Equality and empower women
4) Reduce Child Mortality
5) Improve Maternal health
6) Combat HIV/AIDs, Malaria and other diseases
7) Ensure environmental sustainability
8) Develop a global partnership for development

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110
Q

Smoking is a public health concern, roughly how many deaths are associated with in the UK as of 2016

A

77,900 deaths in the UK in 2016

About 13 deaths per minute in the UK

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111
Q

Explain basic smoking cessation programmes

A

Before consultation - posters and flyer giving risks of smoking and ways to quit

During consultation - ask about their smoking history (pack years), 2% quit with GP advise and 5% quit with repetition, use different theories of behavioural change to help them set a quitting date e.g stages of change (transtheoretical) model

Stop smoking centers - one to one or group sessions, include education on the risks of smoking and different techniques to stop, counselling and also access to medication (nicotine replacement therapy, Buproprion and Varenicline

Medication
Nicotine replacement therapy (NRT) - 12 to 18 years old can only use this, it is contraindicated in those who have had a recent myocadial infarction, arrythmias and stroke

Buproprion (also called Zyban) - used 1 or 2 weeks before stop date of smoking - contraindication in pregnant and breastfeeding women, epileptic, seizures, eating disorders and bipolar disorders

Varenicline (Champix) - use 1 week before stop date of smoking - contraindicated in pregnant women and breast feeding women and those with history of psychiatric illness

Types of smoking cessation services

  • self help materials
  • quitlines (NHS stop smoking service)
  • group behavioural counselling
  • brief interventions by healthcare professionals at GP practice
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112
Q

What is dsynopnea

A

Difficulty breathing or laboured breathing

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113
Q

What is cyanosis

A

Blue colouration to the skin due to poor circulation or inadequate oxygen of the blood

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114
Q

What is haemoptysis

A

Coughing up blood

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115
Q

What is cor pulmonale

A

This is abnormal enlargement of the right side of the hear (right ventricle) due to severe pulmonary hypertension

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116
Q

Would a response to bronchodilators be an indication of asthma or COPD

A

An indication of asthma

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117
Q

Give the aetiology, symptoms and management of COPD

A

COPD is the presence of structural change and narrowing of the small airways due to chronic inflammation, causes a loss of alveolar attachment to small airways and elastic recoil

Aetiology (caused by)

  • cigarette smoking (also including secondhand smoking, cigar and pipe)
  • indoor air pollution (cooking and heating with open fires)
  • outdoor air pollution
  • occupational exposure (fumes, irritants and vapour)
  • alpha 1 antripysin deficiency

Symptoms

  • persistent cough
  • dsynopea (laboured breathing)
  • sputum production
  • wheeze
  • winter exacerbations

Diagnosis
- with a spirometer that measures FEV1, FVC and SVC to produce a scalloped flow-volume loop

Management

  • seen as successful with reduction of exacerbations of disease
  • smoking cessation
  • pulmonary rehabilitation
  • medical managment

Medication used include

  • inhaled broncodilators (SAMA,SABA, LAMA, LABA)
  • oral corticosteroids
  • theophylline
  • mucolytics
  • long term antibiotics
  • long term oxygen therapy and short burst oxygen therapy (in cylinders)
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118
Q

Multidisciplinary team management and interventions

A 
Doctors
Practice nurses
Physiotherapists - lead pulmonary rehabilitation
Respiratory nurse specialists - lead pulmonary rehabilitation
Clinical psychologists
Liaison psychiatrists
Pharmacists
Dieticians
Occupational therapists
Social servics
Assertive outreach nurses
Palliative care experts
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119
Q

What is alpha 1 antitrypsin deficiency

A

This is an autosomal recessive condition

  • alpha1 antitrypsin is a serine protease inhibitor produced by hepatocytes
  • it opposes the alveolar elastase enzyme activity that breaks down alveolar wall and leads to emphysema
  • excess deformed alpha 1 antitrypsin can also build up in the liver and cause liver issues
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120
Q

What is airways restriction and give exmaples

A

Disease that limits inspirations

Pulmonary fibrosis
Asbestosis

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121
Q

What is airways obstruction and give examples

A

Disease that limits expiration

COPD
Asthma
Emphysema
Chronic bonchitis

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122
Q

Give some lung functions tests and their uses

A

Spirometry - measures FEV1, FVC and VC (only direct lung measurement it takes is vital capacity), - simply take a deep breath and exhale as hard and fast as you can - used to create flow-volume loop

Body plethysmography - measures IC, FRC, ERV and vital capacity so total lung capacity can be calculated - sit in a box

Gas dilution (nitrogen washout technique) - measures FRC, all air in lungs - patient breathes in 100% oxygen which displaces nitrogen in lungs, the exhaled nitrogen volume and concentration are measured

Diffusion capacity (DLCO) - measures how well oxygen diffuses from the lungs into blood - patient inhales deep breath from a tube and holds their breath for 10 seconds then exhaled back into the tube which takes a sample of gases, nose clip is worn, inert gas inhaled e.g carbon monoxide

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123
Q

Give the phases of respiratory embryological development

A

Embryonic 0-5 weeks - lung buds enlarge to form right and left main bronchi
Pseudoglandular 5-17 weeks - major airways defined, nests of angiogenesis, cilia formed
Cannalicular 16-25 weeks - terminal bronchioles, capillary beds and alveolar ducts
Alveolar 25 weeks - alveolar budding, thinning and complexification

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124
Q

What is the purpose of the systemic blood vessels

A

To deliver oxygen to hypoxic tissues

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125
Q

What does O2 and CO2 act as in systemic blood vessels

A

CO2 is a vasodilator (hypoxia and acidosis are also vasodilators)

O2 is a vasoconstrictor

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126
Q

What does O2 and CO2 act as in the pulmonary blood circulation

A

O2 is a vasodilator

CO2 is a vasoconstrictor (hypoxia and acidosis are also vasoconstrictors)

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127
Q

What are the surface active phospholipids in surfactant

A

Phosphatidyl choline
Phosphatidyl glycerol
Phosphatidyl inositol
Surfactant proteins A, B, C, D

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128
Q

When is surfactant produced

A

34 weeks from gestation

Large increase 2 weeks prior to birth

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129
Q

What accelerates surfactant production

A

Distension by alveoli
Steriods
Adrenaline

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130
Q

How is surfactant defieciency managed

A 
Warmth
Surfactant replacement (if intubated)
Oxygen and fluids
Continuos positive airways pressure - to maintain lung volumes and reduce the work of breathing
Positive pressure ventilation if needed
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131
Q

What is meant by the term prophylaxis

A

Prophylaxis is a treatment or action taken to prevent a disease developing

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132
Q

Which drug is given for prophylaxis of COPD

A

Tiotropium is given to prevent exacerbation of COPD, it is a long acting anticholinergic bronchodilator

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133
Q

Which drugs are being used to treat deterioration of COPD and what would their role be

A

Steroids - reduced inflammation
Antibiotics e.g amoxicillin - kill bacteria
Oxygen - to increases oxygen intake

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134
Q

Can amoxicillin be taken with food

A

Amoxillin is an antibiotic and can be taken with or without food

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135
Q

What does GTN stand for and what does it do

A

GTN stands for glyceryl trinitrate and it is used to vasodilate the coronary arteries. It increases blood supply to the heart to reduce the risk of myocardial damage and treat myocardial pain (angina)

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136
Q

Give two routes by which GTN is administered to the patient

A

Sublingually (sl)

Transdermally (top)

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137
Q

Why is GTN not used orally

A

-first pass metabolism through the hepatic portal system substantially reduces the bioavailability of the GTN

  • after a drug is swallowed, it is absorbed by the GI tract
  • it enters the hepatic portal system and goes to the liver
  • the liver metabolises many drugs including GTN
  • this first pass reduces the bioavailability of drugs

-however drugs absorbed through the mucosa of the mouth or skin enter the systemic circulation so the sublingual and transdermal routes are preffered

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138
Q

What does PRN on a prescription mean

A

PRN stands for “pro Re Nata” which means use as needed to the maximum advised limit

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139
Q

Give 10 different routes of administration for drugs and their abbreviations

A
  • oral (po)
  • intravenous (iv)
  • rectal (pr)
  • subcutaneous (sc)
  • intramuscular (im)
  • intra-nasal (in)
  • topical or transdermal (top)
  • sublingual (sl)
  • inhaled (inh)
  • nebulised (neb)
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140
Q

Why are salbutamol and clenil modulate administered by inhalation instead of orally

A
  • to avoid first pass metabolism

- so that the drugs get directly into the small airways and exert an effect

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141
Q

Give some routes of administration for ramipril, bendroflumethiazide, amlodipine and lansoprazole

A

Oral (po) for all of them

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142
Q

Give the route of administration for paracetamol

A

Oral (po), rectal (pr) and intravenous (iv)

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143
Q

Give the route of administration for diclofenac

A

Oral (po) , rectal (pr) and topical (top)

144
Q

Give the route of administration for salbutamol

A

Inhaled (inh), nebulised (neb), oral (po) and intravenous (iv)

145
Q

Give the route of administration for clenil modulate

A

Inhaled (inh)

146
Q

What does a patient do with an FP10 and how much is the payment

A

They take it to a chemist or pharmacy in England and it costs 9 pounds

147
Q

Who can complete a yellow FP10D

A

-dentist

148
Q

Who can complete a blue FP10MDA

A

A GP - these are used for drugs like methadone

149
Q

Who can complete a purple or green FP10P, PN, SP or CN

A

Nurses or pharmacists

Im guessing P is pharmacy, SP is supplementary prescriber, CN and PN and nurses

150
Q

What is an FP10

A

It is a prescription that can be completed by a GP, nurse, pharmacy prescriber, supplementary prescriber or hospital doctor in England

151
Q

Who prescribes with a green FP10

A
  • GP
152
Q

What is the minimum information required for a legal prescription for a non-controlled drug

A
  • prescriber’s signature
  • prescriber’s address (usually the practice’s address and usually contains a number to identify individual prescriber)
  • a date
  • patient’s details (name and address)
  • information about the product supplied
153
Q

Give the diameter of the pores of kohns

A

1-2um

154
Q

Which muscle lines the free end of the c shaped cartilage in the trachea

A

The trachealis muscle -it is smooth muscle

155
Q

What are nares

A

The anterior nares are the part of the nose you can put your fingers in

156
Q

What are turbinates and meatus

A

Turbinates are the shelf like structures in the nose

Meatus are the spaces in between the turbinates

157
Q

What is choana

A

The posterior nares

158
Q

Where does the nasolacrimal duct drain into

A

The inferior meatus

159
Q

Name the paranasal sinus, where they drain and their innervation

A

Frontal sinus

  • through the frontonasal duct at the hiatus semilunaris
  • the opthalmic branch of the trigeminal nerve

Sphenoid sinus

  • into the sphenoethmoidal recess in the roof of the nasal cavity
  • the opthalmic branch of the trigeminal nerve

Ethmoidal sinus

  • anterior part into hiatus semilunaris, middle part into the ethmoidal bulla, the posterior part into the superior meatus
  • the opthalmic and maxillary branch of the trigeminal

Maxillary sinus

  • middle meatus
  • maxillary branch of the trigeminal nerve
160
Q

Where does the pharynx begin and end

A
  • begins at the base of the skull

- ends at the cricoid cartilage at C6

161
Q

What does the eustachian tube do

A

Supply air to the middle ear

162
Q

Which two fold contain the palatine tonsils of the pharynx

A
  • the palatoglossal folds

- the palatopharyngeal folds

163
Q

What is the vulvular function of the larynx

A

Prevents liquids entering the lung

164
Q

Give the 9 cartilages of the larynx

A
  • cricoid
  • thyroid
  • epiglottis
  • arytenoid x2
  • cuneiform x2
  • cornicular x2
165
Q

How much air does minute ventilation transport

A

5 litres

166
Q

How much gas exchange area is there in each lung

A

20m2 area per lung

167
Q

Where does the trachea start and end

A

From C6 to T5 at the carina

168
Q

What is the difference between the larynx and the trachea

A
  • larynx is in the upper part of the trachea

- larynx is called the voice box

169
Q

Where does the larynx start and finish

A

Starts at C3 and finishes at C6

170
Q

How long is the right main bronchus

A

1-2.5cm

171
Q

How long is the left main bronchus

A

5cm

172
Q

How many orders of branching does the pulmonary arteries have

A

17

173
Q

For inspiration to occur, will the intra-alveolar pressure be positive or negative

A

Negative

174
Q

How many alveoli are in one lung

A

300,000,000 per lung

175
Q

How many capillaries per alveolus

A

1000

176
Q

At rest, when haemoglobin fully saturated with oxygen

A

25% way through

177
Q

What is dead space

A

Volume of inspired air not contributing to ventilation

178
Q

CO has how much greater affinity for Hb than O2

A

200 times

179
Q

How does CO influence the curve shift

A

CO causes the curve to shift to the left and loss of the sigmoid shape occurs

180
Q

Factors that affect Peak Flow

A

Age
Gender
Height

181
Q

What does spirometry measure

A

Tbc

182
Q

What does the peak flow measure

A

Tbc

183
Q

Give the two types of NHS press releases and examples

A

Reactive: defending the NHS reputation e.g.

  • following news reports of infection control issues
  • increased mortality at specific hospitals
  • justifying why an expensive monoclonal antibody was not funded

Proactive: Improve and protect population health e.g.

  • social marketing messages (five-a-day, change for life campaign)
  • emergency preparedness
  • early recognition and symptom awareness (act FAST)
184
Q

Give 3 examples of vaccine preventable communicable diseases

A

Measles
Mumps
Rubella

185
Q

Why do people smoke

A

-influence of background (smoking in parents, siblings, peers; relatively deprived neighbourhoods; schools where smoking is common)
-tightly regulated addiction
•Individual differences
•Social, economic, personal, and political influences all play an important part in determining patterns of smoking prevalence and cessation
•Behaviour, habit, cues

186
Q

Give the physical and psychological effects of nicotine making it addictive

A

Physical

  • nicotine activates the nicotinic acetylcholine receptors in the brain and cause a release of dopamine in the nucleus accumbens
  • it is a stimulant and tolerance can be built to it

Psychological
-withdrawal can be experienced

187
Q

What has been identified as the biggest cause of inequality of death rates in the rich and poor in the UK

A

Smoking

188
Q

Estimated cost of smoking to the NHS (2019)

A

2.4 billion pounds

189
Q

Total cost of smoking to society

A

12.5 billion pounds

190
Q

Cost of loss of productivity due to smoking breaks at work

A

3.3 billion pounds

191
Q

Cost of absences from work (absenteism)

A

1.3 billion pounds

192
Q

Give a study that shows evidence that smoking causes early death and disease

A

The 1951 doctor study

After a 40 year follow up (by 1991) they found that the non smokers had 80% who lived till 70 and 33% who lived till 85. They found that the smokers had 50% who lived till 70 and 8% who lived till 85

193
Q

Detail the 2007 smoking ban in public places law

A
  • the legal minimum age for buying tobacco products was raised to 18 in the great britain
  • it was made illegal to smoke in enclosed public places except bus shelters, hotel rooms, nursing homes and psychiatric ward (till july 2009)
194
Q

When was it made illegal to display tobacco products in large stores and small stores

A

In large stores - 2012

In small stores - 2015

195
Q

When was it made illegal to smoke in cars containing children

A

2015

196
Q

In May 2017, what law was imposed on smoking companies

A

-standardised packaging was introduced where tobacco companies had to cover 65% of the packet with health warnings

197
Q

Who and when was the first report on smoking and carcinoma of the lung published in the British Medical Journals

A

1950, Richard Doll and Austin Bradford-Hill

198
Q

When did parliament ban cigarette advertising on TV

A

In August 1965

199
Q

What did the 1986 act do

A

The 1986 protection of children (Tobacco) Act amended the children and young persons Act 1933 to make it an offense to sell tobacco products to under 16

200
Q

Give some types of nicotine replacement therapy

A
  • patches
  • gum
  • lozenges
  • nasal sprays
  • microtab
  • inhalers
201
Q

Give some non-nicotine pharmacological interventions for smoking

A
  • buproprion (zyban)

- varenicline (champix)

202
Q

Are more people more or less likely to smoke

A

Less likely to smoke

203
Q

Where can IgA be found

A

In mucus secretions and mucus membranes

204
Q

What are epitopes and paratopes

A

Epitopes are the part on an antigen that the antibodies attach to

Paratopes are the specific (varible) region on an antibody

205
Q

Which conditions are type 1 hypersensitivity associated with

A
  • asthma
  • anaphalaxis
  • hayfever
  • peanut allergy
206
Q

Which conditions are type 2 hypersensitivity associated with

A
  • triggered by immunoglobulins bound to surface antigens
  • good pastures syndrome
  • non-respiratory e.g Grave’s disease and myaesthenia gravis
207
Q

Which conditions are type 3 hypersensitivity associated with

A
  • formation of precipitating antibodies to organic dusts, the granulomata then heal by fibrosis
  • antibodies and targets circulate (e.g. chronic bacterial endocarditis). Little lumps of antibody and target get deposited in the skin, lung, kidneys etc and activate immunity, resulting in tissue damage
  • lupus (SLE)
  • farmer’s lung
  • pigeon fancier’s lung
  • malt worker’s lung
  • mummy handler’s lung
  • snuff-taker’s lung
  • rat handler’s lung
  • woodworker’s lung
  • basement lung
  • humidifier lung (amoebae)
  • cheese-washer’s lung
  • paprika slicer’s lung
  • compost lung
208
Q

What causes type 3 hypersensitivity

A

-formation of precipitating antibodies to organic dusts, the granulomata then heal by fibrosis

209
Q

What causes type 4 hypersensitivity

A
  • formation of granulomas, slow process, granulomas are little walled-off areas nailing nasty things in place
  • dependent upon activation of T cells
210
Q

Which conditions are type 4 hypersensitivity associated with

A
  • sarcoIdosis

- TB

211
Q

Give the causes of hypoxaemia

A
  • alveolar hypoventilation
  • reduced PiO2
  • ventilation/perfusion mismatching (v/q)
  • diffusion abnormality
212
Q

Give the alveolar gas equation

A

PAO2= PiO2 - PaCO2/R

213
Q

Give 3 ways CO2 is carried in the blood

A
  • bound to haemoglobin (23%)
  • dissolved in plasma
  • as HCO3-
214
Q

What are the physiological causes of high CO2

A
  • alveolar ventilation (v’A) is reduced due to reduced minute ventilation
  • alveolar ventilation due to increase in dead space ventilation by rapid shallow breathing
  • alveolar ventilation due to increased dead space ventilation by V/Q mismatching
  • increased CO2 produced
215
Q

Give the pH range of blood

A

Ph 7.35-7.45

216
Q

What is the pH of blood

A

Ph 7.4

217
Q

Give a weak acid and weak base in the body

A
  • HCO3- weak base

- H2CO3 weak acid

218
Q

Give the 3 main buffering systems used to regulate pH of the body fluids (blood)

A
  • intracellular and extracellular buffers
  • the lungs eliminating CO2
  • renal HCO3- reabsorption and H+ elimination
219
Q

Give an example of a volatile acid produced by metabolic processes in the body and how it is excreted

A
  • carbonic acid

- equilibrium with CO2 and excreted by lungs as CO2

220
Q

Give examples of non volatile (fixed) acids produced by metabolic processes in the body and how they are controlled in the body

A
  • sulphuric acid, hydrochloric acid
  • these are not eliminated by the lungs
  • buffered by body proteins or extracellular buffers then excreted by renal systems
221
Q

What does the Henderson-Hasselbalch equation calculate

A

-pH

222
Q

What does the HCO3- and the PCO2 in the Henderson-Hassel balch equation reflect

A
  • HCO3- reflects the generation of non-volatile acids buffered an eliminated by renal system
  • PCO2 reflects dissolved CO2 in the blood and its elimination by the lungs
223
Q

Compensation for respiratory acidosis

A

-as PCO2 rises, HCO3 must rise so renal compensation (produces HCO3-)

224
Q

What would be observed in respiratory acidosis

A
  • increased PaCO2
  • decreased pH
  • mild increased HCO3-
225
Q

What would be observed in respiratory alkalosis

A
  • decreased PaCO2
  • increased pH
  • mild decreased HCO3-
226
Q

What would be observed in metabolic acidosis

A
  • reduced bicarbonate HCO3-

- decreased pH

227
Q

What would be observed in metabolic alkalosis

A
  • increased bicarbonate

- increased pH

228
Q

Give examples of endocytic pattern recognition receptors

A
  • mannose receptors
  • glucan receptors
  • scavenger receptors
229
Q

How many neutrophils are made each minute

A

80 million

230
Q

Give the primary and secondary granules of a neutrophil

A

Primary

  • myeloperoxidase
  • elastase
  • cathepesins
  • defensins

Secondary

  • receptors
  • lysozymes
  • collagenase
231
Q

Which membrane enzyme generates ROS

A

-NADPH oxidase generates reactive oxygen species (ROS)

232
Q

Give an example of an X linked and an autosomal recessive condition that cause the generation of the reactive oxygen species (ROS)

A
  • cytochrome B91KD (X linked)

- P47 cytosolic factor (autosomal recessive) - interferon restores P47 activity

233
Q

At the end of the 5th week, a septum divides the foregut and airways, what is it called

A

-the transoesophageal septum (also called the oesphago-tracheal septum)

234
Q

Give fetal blood circulation

A

Think 1, 2, 3

  • 1 umbilical vein (becomes ligamentum tere)
  • 2 umbilical arteries (become medial umbilical ligaments)
  • 3 fetal shunts which are ductus venosus, foreamen ovale and ductus arteriosus (become respectively
235
Q

What is surface tension

A

A measure of the force acting to pull a liquid’s surface molecules together at an air-liquid interface

236
Q

What is COPD

A
  • Persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory response
  • Mixture of small airway disease and parenchymal destruction
  • Small airways collapse due to destruction of pulmonary elastic tissue causing further obstruction

Main symptoms are shortness of breath, persistent cough and sputum production

237
Q

What is asthma

A
  • Excess mucous secretions lead to narrowing of the airways increasing airway resistance
  • Voluntary respiratory effort increases which in turn increases resistance and causes small airways to collapse
  • FRC increases leaving over expanded lungs
238
Q

What is emphysema

A
  • Enlargement of the alveolar sacs by the destruction of alveolar walls
  • Reduced surface for gas exchange
  • Reduced oxygenation of blood
239
Q

What is a pulmonary arterial wedge pressure and what does it measure (include the formular)

A
  • balloon on a catheter pushed from peripheral vein into the right atrium, right ventricle and then into the pulmonary artery then inflated
  • used as an indirect estimate of left atrial pressure

mPAP - PAWP = CO x PVR

mPAP is mean pulmonary arterial pressure
PAWP is pulmonary arterial wedge pressure

240
Q

How does hereditary pulmonary arterial hypertension affect the individual

A
  • endothelial dysfunction

- smooth muscle proliferation

241
Q

Give 3 respiratory condition that single gene changes are responsible for, include the gene responsible, its function and the pattern of inheritance

A
  • cystic fibrosis, CFTR, Cl-ion transport channel, autosomal recessive
  • alpha-1-antitrypsin deficiency , SERPINEA1, anti-protease, autosomal recessive
  • hereditary pulmonary arterial hypertension (HPAH), BMPR2, endothelial dysfunction and smooth muscle proliferation, autosomal dominant
242
Q

What percentage of pulmonary arterial hypertension carriers develop it (penetrance)

A

-20% of carriers develop it

243
Q

In first aid, what does a coherent answer to “are you okay” indicate

A
  • that the airways are clear
  • breathing ok
  • circulation is perfusing the brain
244
Q

In first aid, give 3 ways you would conduct an initiate assessment and collect information

A

DRABC, DOTS and SAMPLE

Danger
Response
Airways
Breathing
Circulation

Deformities
Open wounds
Tenderness
Swellings

Signs and symptoms
Allergies
Medication
Past medical history
Last oral intake (food and drink)
Event leading to injury or illness
245
Q

What is a seizure

A

-uncontrolled electrical activity in the brain which may produce physical convulsions

246
Q

What is epilepsy and how many people are diagnose with it each year

A
  • epilepsy is the tendency of recurrent seizures

- 87 people are diagnosed with epilepsy every day?

247
Q

Causes of epilepsy

A
  • post head injury
  • flashing lights
  • alcohol poisoning
  • drugs
  • hypoglycemia (low blood sugar)
  • brain tumour
  • infection/hyperpyrexia
  • lack of oxygen
248
Q

When do you call 999 in a seizure

A
  • if its their first one
  • lasts longer than 5 minutes
  • repeated seizures occur
  • unresponsive for more than 10 mins after seizure
  • injury occurs
249
Q

What is a syncope (fainting)

A

-loss of consciouness due to temporary reduction in blood flow to the brain

250
Q

When should 999 be called with syncope

A

-if consciousness is not regained within two minutes

251
Q

What are the types of burns that can be sustained

A
  • dry burn caused by naked flames, friction, hot water bottles in diabetic neuropathy
  • a scald caused by wet heat e.g steam or a cup of tea
  • radiation burns e.g sunburn or radiotherapy
  • cold burns e.g frostbite
252
Q

How much do burn accidents cost the NHS a year

A

20 million pounds per year

253
Q

Give the classification of burns

A
  • superficial -outer layer of the skin
  • partial thickness - all layers of the skin
  • full thickness - tissues and structures under the skin e.g muscles and nerves
254
Q

When do you call 999 with a burn

A
  • when it is bigger than the size of the casualty’s hand
  • it is on the face, hands, feet or genitals
  • it involved the airways (mouth and or nose)
  • it is a full thickness burn
  • it extends around a limb
255
Q

What is a fracture and the difference between closed and open fracture

A
  • a fracture is a crack or break in a bone
  • a closed fracture is where the damage to the bone is under the skin
  • an open fracture occurs when pieces of bone puncture the skin
256
Q

What does a splint do in a fracture

A
  • support an injured limb
  • immobilise the injury
  • reduce pain
  • prevent further damage to nerves and blood vessels
257
Q

What is shock

A

-a critical condition that is brought on by a sudden drop in blood flow through the body

258
Q

What can cause shock

A
  • heart attack or heart failure
  • fluid loss from bleeding, dehydration, diarrhoea, vomiting or burns
  • anaphylaxis
  • blood vessel failure
259
Q

What are the two main types of strokes

A

Ischaemic stroke and haemorrhagic stroke

  • ischaemic stroke - 80% of strokes are ischaemic, occurs when an artery supplying part of the brain is blocked, starving the distal brain tissue of the oxygen
  • haemorrhagic stroke - occurs when a blood vessel in the brain bursts and the bleeding puts pressure on the brain tissue
260
Q

What does FAST stand for

A

Face
Arms
Speech
Time

261
Q

Where can a sample of arterial blood be taken from and what can be measured

A
  • radial, brachial and femoral artery

- PaO2, PaCO2, pH [H+] acidity, HCO3- bicarbonate

262
Q

Give the determinants of PaCO2 and PaCO2 equation

A

-alveolar ventilation
PaCO2 = 1/alveolar ventilation
PaCO2 = kV’CO2/ V’A

263
Q

Give an alveolar gas equation that does not take into account pH2O

A

PAO2 = PiO2 - PaCO2/R

R is the respiratory quotient and is the CO2 produced/O2 consumed

264
Q

What is the respiratory quotient (R) normally and how does it change with a carbohydrate or fatty diet

A
  • normally 0.8 with normal diet
  • 1 with a high carbohydrate diet
  • 0.7 with a fat rich diet
265
Q

What is minute ventilation

A
  • volume of air breathed in and out in one minute

- usually about 5 litres

266
Q

What is pulmonary barotrauma

A 
-air leaks from burst alveoli
causing
-pneumothorax
-pneumomediastinum - air leaked into the mediastinum
-subcutaneous emphysema 
-problem with pressure
267
Q

What is arterial gas embolism (AGE)

A
  • gas enters circulation via torn pulmonary veins
  • small transpulmonary pressure can lead to arterial gas embolism
  • normally occurs within 15 mins of surfacing
  • need urgent recompression
  • problem with pressure
268
Q

What is decompression illness

A
  • ascent causing fall in pressure and solubility
  • causes gas bubbles in different parts of the body

Type 1 is cutaneous only
Type 2 is neurological

269
Q

What is inert gas narcosis

A
  • most common is nitrogen narcosis
  • worsens with increasing pressure
  • increased PiN2
270
Q

What is the normal range for PaO2

A

11-13kPa

271
Q

How much of the drug warfarin is bound to plasma proteins and how much is freely dissolved in plasma and is it the free warfarin or the plasma bound warfarin that is responsible for the cation of the drug

A

99% of warfarin is bound to plasma proteins and 1% is free in plasma.
The free warfarin (1%) is responsible for the action of the drug

272
Q

What happens if tamoxifen is given to a patient taking warfarin

A

Tamoxifen increases the effects of warfarin and so increases the risk of bleeding by an unknown mechanism

273
Q

The active metabolite of tamoxifen, 4-hydroxytamoxifen, competitively binds to the intracellular oestrogen receptor. What is meant by competitive binding?

A

Competitive binding means that both the tamoxifen and oestrogen bind (‘compete for’) to the same oestrogen receptor

-if 4-hydroxytamoxifen bind to the oestrogen repceptor, it prevents oestrogen binding so reduces the effects of oestrogen.

274
Q

How does warfarin affect vitamin K in the liver

A

-warfarin blocks the effects of vitamin K in the liver

275
Q

What substances are produced in the liver using vitamin K and what is the effect of blocking the action of vitamin K

A

Vitamin K is used within the liver to make clotting factors 2, 7, 9 and 10 (think 1972)

Blocking the action of vitamin K leads to an inability to form blood clots efficiently

276
Q

What is the effect of drinking alcohol whilst on warfarin and how does this affect clotting

A
  • drinking can increase the anticoagulant effects of warfarin causing bleeding
  • drinking can affect the ability of the liver to manufacture the clotting factors 2, 7, 9 and 10 (think 1972)
277
Q

What route of administration is used to deliver the betamethasone to the diseased skin and what implications does this delivery have on possible systemic side effects

A
  • betamethasone is delivered topically on skin
  • an advantage to this is that a high dose is delivered to diseased skin and small dose enters the systemic circulation
  • systemic effects of topical steroids can include hypothalamic pituitary adrenal axis suppression, Cushing’s syndrome, diabetus mellitus, osteoporosis and growth retardation in children
  • less than 2% of the topical steroid is absorbed systemically
  • penetration is related to the thickness of the stratum corneum at the site of application
278
Q

How can we increase the efficacy of betamethasone without increasing the dose and what other skin products can exacerbate eczema

A
  • to increase efficacy,
  • drugs in aqueous cream will absorbed different to drugs in paraffin based ointment
  • using an occlusive dressing can increase absorption by up to 10 times
  • vigorous rubbing increases local blood supply an increase systemic absorption
  • zerobase emollient cream can cause local skin or allergic reactions
  • perfumed creams, shower gels or bubble baths can exacerbate eczema
279
Q

Give the environmental influences of asthma

A
  • pollens
  • infectious agents
  • fungi
  • pets
  • animals
  • air pollution
280
Q

Give the occupational influences of asthma

A
  • car spray paints
  • resins
  • cleaning agents (low molecular weight agents)
  • laboratory animal workers (high molecular weight agents)
  • wood dust
281
Q

What is hypersensitivity pneumonitis

A
  • an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled dusts
  • hot tub lung is a disease example of this condition
282
Q

What are the 10 principles of screening according to Wilson and Jungner

A

Wilson and Jungner classic screening criteria

  1. The condition sought should be an important health problem.
  2. There should be an accepted treatment for patients with recognized disease.
  3. Facilities for diagnosis and treatment should be available.
  4. There should be a recognizable latent or early symptomatic stage.
  5. There should be a suitable test or examination.
  6. The test should be acceptable to the population.
  7. The natural history of the condition, including development from latent to declared disease, should be adequately understood.
  8. There should be an agreed policy on whom to treat as patients.
  9. The cost of case-finding (including diagnosis and treatment of patients diagnosed) should be economically balanced in relation to possible expenditure on medical care as a whole.
  10. Case-finding should be a continuing process and not a “once and for all” project.
283
Q

Have an awareness of the NHS bowel cancer screening program and other cancer screening programs

A

Screening in pregnancy

  • sickle cell and thalassaemia (10 weeks)
  • infectious diseases (HIV, hepatitis B and syphillis)
  • Down’s syndrome, Edwards’ syndrome and Patau’s syndrome
  • 11 physical conditions in the baby (20 week scan)

Newborn screening - newborn blood spot test and physical examination
Diabetic eye screening - offered annually to diabetics who are 12 and over
Cervical screening - offered to women aged 25 to 49 every 3 years, aged 50 to 64 every 5 years
Breast screening - offered routinely to women from 50 to 71st birthday
Bowel cancer screening -offered to men and women aged 60 to 74 every 2 years
Abdominal aortic aneurysm (AAA) screening - offered to men when they turn 65

284
Q

Give 8 red flag symptoms for bowel cancer

A
  • weight loss
  • palpable mass on rectal/abdominal examination
  • night sweats
  • fever
  • change in bowel habits
  • lethargy/malaise
  • faecal incontinence
  • nocturnal diarrhoea
285
Q

Is the first part of expiration active or passive

A

Active

-active slowing of inspiration

286
Q

During ascent which remains constant and which changes in FiO2 and PiO2

A

FiO2 remains constant

PiO2 decreases

287
Q

How does ascent in altitude affect control of respiration (at 10,000 feet)

A
  • hypoxia leads to
  • hyperventilation
  • increases minute ventilation
  • lowers PaCO2
  • alkalosis initially but compensated for by renal bicarbonate excretion
  • tachycardia
288
Q

What is extremely high altitude

A

-over 18,000 feet

289
Q

What are the normal blood gas ranges at sea level

A

PaO2 10.5 - 13.5 kPa
PaCO2. 4.6 - 6 kPa
pH 7.36 - 7.44

290
Q

What are the blood gas ranges at Everest

A

PaO2 4 kPa
PaCO2. 1.5 kPa
pH 7.56

291
Q

Give examples of 3 high altitude illnesses

A
  • acute mountain sickness
  • high altitude pulmonary oedema (HAPE)
  • high altitude cerebral oedema (HACE)
292
Q

Definition of acute mountain sickness

A
  • lake louise score of 3

- must have a headache and one other symptom

293
Q

How do you treat acute mountain sickness

A

-descent from high height

294
Q

How to treat high altitude pulmonary oedema

A
  • O2
  • descent
  • gamow bag
  • steroids
  • Ca2+ blockers
295
Q

If the total lung capacity in a 23 year old female diver is 8 litres at the surface. What will this volume be at 160m of seawater during breath hold diving?

A 
Use Boyle's law which is P1V1 = P2V2
1 atm x 8 litre =17 atm x V1
1 x 8 = 17 x V
8 = 17 x V
8/17 = V
V = 0.470 litres which is 470 mls

Think 160/10 is 16, then add 1 (sea level atm) to the 16 = 17

296
Q

What is pulmonary barotrauma

A 
- air leaks from burst alveoli
Causes
-pneumothorax
-pneumomediastinum (air leaks into the mediastinum)
-subcutaneous emphysema
-problem with pressure
297
Q

What is an arterial gas embolism (AGE)

A
  • gas enters circulation via torn pulmonary vein
  • small transpulmonary pressure can lead to arterial gas embolism
  • normally occurs within 15 mins of surfacing
  • urgent recompression
  • problem with pressure
298
Q

What is decompression illness

A

Ascent causing fall in pressure and solubility of gases
-causes gas bubbles in different parts of the body

Type 1 is cutaneously only
Type 2 is neurological

299
Q

What is inert gas narcosis

A
  • most common is nitrogen narcosis
  • worsens with increasing pressure
  • increased PiN2
300
Q

Give 5 known occupational causes of COPD

A
  • silica
  • coal
  • grain
  • cotton
  • cadmium
301
Q

Give some symptoms of CNS oxygen toxicity

A

Think ConVENTID

Convulsions
Visions
Ears ringing
Nausea
Twitching
Irritability
Dizziness
302
Q

What is pulmonary oxygen toxicity

A
  • Lorrain smith effect is noticed
  • PiO2 > 0.5ATA
  • a common problem with intensive care uni patients on 100% oxygen
  • relieved by PiO2 <0.5 ATA
  • FVC can be useful to monitor
303
Q

What is the partial pressure of nitrogen and oxygen at sea level and at 10 meters of sea water due to Dalton’s law

A

At sea level - partial pressure N2 = 0.78, O2 = 0.209
At 10 meters of sea water - partial pressure N2 = 1.56, O2 = 0.418

Breathing air at 10 msw (meters of sea water) is the same PaO2 as breathing 42% (instead of 21%) O2 at sea level

304
Q

What is Dalton’s Law

A

Total pressure exerted by a mixture of gasses is equal to the sum of the pressure that would be exerted by each of the gases if it alone were present and occupied the total volume

305
Q

What are the physiological changes caused by the diving reflex

A
  • apnoea
  • bradycardia
  • peripheral vasoconstriction
306
Q

What is Henry’s Law

A

The amount of a gas dissolved in a liquid at a given temperature is directly proportional to the partial pressure of the gas

307
Q

What are the effects of henry’s law

A
  • proportionally more gas dissolves in the tissue at depth
  • if ascent is at a rate that exceeds the body’s capacity to clear the excess gas, then inert gas bubbles may form in the tissues leading to decompression illness
308
Q

What is Boyle’s law

A

-at constant temperature the absolute pressure of a fixed mass of gas is inversely proportional to its volume

309
Q

1 atmosphere absolute (ATA) is equal to

A
  • 10 metres of sea water (msw)
  • 33 feet of sea water (fsw)
  • 101.3 kilopascals (kPa)
  • 760 mmHg/torr
  • 1000 millibars
310
Q

How is PiO2 caculated

A

PiO2 (PiGas) = Patm x FiO2 (FiGas)
PiO2 = 100kPa x 0.21
PiO2 = 21kPa at sea level

311
Q

How can PaO2 be calculated

A

PaO2 = PAO2 - (A-aDO2)

  • calculate the alveolar gas equation to get PAO2
  • then put PAO2 in the equation
  • PaCO2 can be measured in the alveolar gas equation from arterial blood gas
312
Q

Give the barometric pressure kPa for the following altitude (metres) 0, 4800, 6300, 8100 and 8848

A
  • 0m = 101kPa
  • 4800m = 57kPa
  • 6300m = 46kPa
  • 8100m = 37.5kPa
  • 8848m = 33.5kPa
313
Q

What is somatic hyper-mutation

A

-exposure to relevant antigen triggers replication with errors in variable region DNA replication generating further diversity

314
Q

What is immune tolerance

A

-a state of unresponsiveness of the immune system to antigens that normally have the capacity to elicit an adaptive immune response

315
Q

What leads to autoimmune disease

A

-failure to establish self-tolerance leads to autoimmune disease where our immune system attacks our own antigens e.g rheumatoid arthriti, systemic lupus erythematosis

316
Q

What is affinity maturation in adaptive immunity

A

-selection for higher affinity clones

317
Q

What is the basis of diversity and specificity in immunity

A

-generation of pathogen-specific variable regions in lymphocyte receptors

318
Q

What is central and peripheral tolerance in adaptive immunity

A
  • central tolerance is in the thymus or bone marrow, lymphocytes that react with self antigens are deleted or develop into suppressor ‘Tregs’ (T helper cells)
  • peripheral tolerance is in the lymph nodes, autoreactive clones escaping central tolerance are deleted or suppressed by ‘Tregs’ (usually in lymph gland, lymph tissue and circulation)
319
Q

How are memory cells distinguished from naive cells

A
  • high affinity receptors
  • increased lifespan
  • faster and stronger response to stimulation
320
Q

How does antigen presenting cells activate T cytotoxic cells

A
  • antigen presenting cell (APC) ingests bug
  • bug antigen is displayed on APC cell surface with MHC1 (major histocompatibility complex 1) molecule. Both must be recognised
  • CD8 cells activated to become cytotoxic
321
Q

How do activated cytotoxic T cells kill their target

A
  • they kill pathogen-infected or tumour cells by pore formation
  • cytotoxic T cell binds to infected cell
  • perforin makes holes in infected cell’s membrane
  • infected cell lyses
322
Q

What can defective cytotoxic T cell responses lead to

A
  • increase viral infections

- may promote progression of cancer

323
Q

How do antigen presenting cells activate T helper cells

A
  • antigen presenting cells (APC) ingests bug
  • bug antigen displayed on APC cells surface with MHC2 (major histocompatibility complex 2) molecule. Both must be recognised
  • interactions with T cell receptors and co-inhibitory/co-stimulatory receptors releases cytokines
  • CD4 cells differentiate into a range of T helper subtypes - Th1 cell, Tfh cell and Th2 cell
324
Q

What is the principle of necessity

A

Tbc

325
Q

What are IgE associated with

A
  • mast cells

- allergic reactions

326
Q

What IgG associated with

A
  • make up more than 80% of circulating antibodies

- interact with phagocytes

327
Q

What are IgA associated with

A
  • mucosal immunity (gut and lung)

- good at opsonising (promotes phagocytosis) and fixing complement

328
Q

What are IgM associated with

A
  • immature plasma cells secrete IgM
  • IgM is always present in early immune response
  • good at neutralising and agglutinating
329
Q

Give 4 effector functions of antibodies

A
  • neutralisation. - antibodies cover biologically active portion of microbe or toxin
  • agglutination - antibody cross-links cells forming clumps
  • opsonisation - FC region of antibody binds to receptor of phagocytic cels triggering phagocytoses
  • complement fixation - FC region of antibody binds complement proteins so complement is activated
330
Q

What are vaccines derived from

A
  • dead or attenuated bacteria
  • capsular polysaccharide
  • viral proteins
331
Q

In immunity, failure to eliminate pathogens lead to

A

-chronic inflammation

332
Q

In immunity, failure of antibody production leads to

A

-recurrent or severe bacterial infection

333
Q

In immunity, failure of tolerance leads to

A

-autoimmune disease

334
Q

In immunity, failure of T cell function leads to

A

-opportunistic infections such as bacteria, parasites, fungi, viruses and tumours

335
Q

Which cells are infected by HIV virus

A

-CD4+ (T helper cells)

336
Q

What is an antigen

A

-a molecule capable of inducing a specific immune response on the part of the host organism.
Can be
-proteins
-polysaccharides
-lipids
-DNA
Can be soluble or part of cell or pathogen

337
Q

Give 3 conditions from failure of tolerance

A
  • rheumatoid arthritis (anti-citrullinated proteins)
  • graves disease (anti-TRH receptors)
  • vasculitis (anti-neutrophil)
338
Q

How is diversity generated in early development via DNA rearrangements

A
  • through VDJ recombination
  • all but one of each of V (50 variable), D (27 diversity) and J (6 joining) segments in both the heavy and light chains)
339
Q

What is a malignant tumour of the pleura membrane called

A

A mesothelioma

340
Q

the main peripheral chemoreceptors are located in

A

the carotid arteries and aortic arch

341
Q

Changes in oxygen, carbon dioxide and H+ ions stimulates which chemoreceptor

A

Carotid chemoreceptors

342
Q

Give some conditions that cause type 1 respiratory failure

A
  • pulmonary embolism
  • pneumothorax
  • pneumonia
343
Q

Give some conditions that cause type 2 respiratory failure

A
  • COPD

- severe motor neurone disease

344
Q

Does adrenaline cause bronchodlation

A

Yes

345
Q

Would someone with chronic type 2 respiratory failure have a high or low HCO3-

A
  • a high HCO3-
  • because their body would have become accustomed to the high PaCO2 levels which would initially cause a low HCO3- but after time the body would make it high again
346
Q

How does rheumatoid arthritis affect the lungs

A
  • in rheumatoid arthritis, autoantibodies are formed against modified (e.g citrullinated) proteins in joints
  • smoking induces citrullinated proteins in the lungs
  • autoantibodies may cause lung epithelial injury
347
Q

What is positive vasculitis (ANCA)

A
  • anti-neutrophil cytoplasmic antibodies (ANCA)
  • overactive neutrophil which attack blood vessels in various organs particularly the kidney and lung
  • can cause glomerulonephritis and pulmonary haemorrhage
348
Q

What causes inflammation to be chronic

A

A persistent initiating cause

  • persistant infection e.g mycobacteria, abscess
  • persistent irritant e.g smoking, gall stones
  • foreign bodies e.g inhalation of food

Inappropriate cellular response

  • autoimmunity e.g rheumatoid arthritis
  • granulomatosis disease e.g sarcoidosis

Structural abnormalities

  • bronchiectasis e.g local defences malfunction
  • diverticular disease
349
Q

What are the consequences of chronic inflammation

A
  • systemic e.g malaise, weight loss, fever, sweats, anaemia
  • tissue destruction e.g cavity formation
  • fibrosis e.g strictures, organ dysfunction
  • growth disorders like metaplasia, neoplasia e.g carcinoma of the bronchus in pulmonary fibrosis
350
Q

What is bronchiectasis

A

-dilated, scarred airways

351
Q

What are the 3 patterns of chronic inflammation

A
  • chronic suppurative inflammation (mainly innate cells e.g neutrophils)
  • chronic autoimmune inflammation (mainly adaptive cells, can lead to fibrosis)
  • chronic granulomatous inflammation (mainly adaptive cells, can lead to fibrosis)
352
Q

Lung abscess are an examples of which pattern of chronic inflammation

A

-chronic suppurative inflammation

353
Q

What are granulomas

A

-small nodules composed of organised collections of macrophages, ‘epitheliod’ and giant cells

354
Q

Give 3 causes of chronic granulomatous inflammation

A
  • infections (tuberculosis)
  • foreign bodies (inhaled antigens in hypersensitive pneumonitis)
  • aberrant inflammation (vasculitis, Crohn’s disease)
  • unknown (sarcoidosis)
355
Q

Give 4 causes of chronic lung abscesses

A
  • organism (staplylococcus)
  • obstruction (tumour or inhaled foreign bodies)
  • tissue damage (aspiration of gastric contents)
  • impaired immune system (e.g diabetes)
356
Q

Define respiratory failure.
Define type 1 respiratory failure and its causes. Define type 2 respiratory failure and its causes. Which type does Mary have?
Which type does her sister have? 


A

Respiratory failure is when not enough blood is passing from your lungs into the blood or when not enough carbon dioxide is not being removed from the blood

Type 1 respiratory failure is cause by low oxygen in the blood (hypoxemia) and normal or low CO2 (hypocapnia)
PaO2 < 8Kpa
PaCO2 < 6Kpa
Causes of type 1 respiratory failure are;
- Pulmonary oedema
- Pnuemonia
- Acute respiratory distress syndrome (ARDS)
- Chronic pulmonary fibrosis alveolitis
- V/Q mismatch due to alveoli hypoventilation
- High altitude
- Shunt
- Diffusion problem

Type 2 respiratory failure is low blood oxygen (hypoxemia) and high blood CO2 (hypercapnia)
Causes of type 2 respiratory failure are;
- COPD
- Respiratory muscle weakness (Guillian-Barre syndrome)
- inadequate alveoli ventilation due to reduced breathing effort
- Depression of central respiratory centre (heroin overdose)
- Neuromuscular problems

357
Q

Describe the control of respiration

A

Medulla Oblongata
Dorsal respiratory group (DRG)
- Dorsal respiratory group neurons fire through the spinal motor neurones to activate the inspiratory muscles to contract (diaphragm and intercostal muscles)

Ventral respiratory group (VRG)

  • the respiratory rythmn generator is located in the pre-Botzinger complex of the upper part of the ventral respiratory group, it maintains the basal respiratory rate
  • During quiet breathing, VRG neurons activate inspiratory muscle contraction
  • Neurons fire when large increase in ventilation needed e.g exercise
  • In active expiration, VRG neurones cause expiratory muscles to contract e.g pectoralis major, pectoralis minor

Both are bilateral and project into the bulbo-spinal motor neurone pools
Dorsal respiratory group is active during inspiration
Ventral respiratory group is active during inspiration and expiration

Pons

  • apneustic centres - in the lower part of the pons and causes inspiration
  • pneumotaxic centre (pontine respiratory group) - in the upper part of the pons and it swiches off inspiratory muscles to prevent hyperinflation which then causes exhalation

Flascards (17 decks)

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