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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 13 and 14 - Allergic Airway Disease and Hypoxia > Flashcards

RS Lecture 13 and 14 - Allergic Airway Disease and Hypoxia Flashcards

1
Q

What are the 3 allergic airway regions of disease?

A

Upper airways (allergic rhinitis), Bronchi (asthma), alveoli (allergic alveolitis)

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2
Q

How do we distinguish an allergy from hypersensitivity?

A

Is immunological -> so are IgE-mediated

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3
Q

What is allergy?

A

An exaggerated immunological response to a foreign substance which is either inhaled, swallowed, injected or comes in contact with the skin/eye -> a mechanism NOT a disease

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4
Q

What are some diseases that have allergy mechanisms?

A

Plays an important role in some diseases all the time; but in others only some of the time

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5
Q

What are the 2 immune pathways and which one has gone wrong to produce allergy?

A

The pathway for helminths and parasites -> IgE

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6
Q

What is Atopy?

A

Hereditary predisposition to produce IgE Ab against common env allergens -> allergic rhinitis, asthma, atopic eczema

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7
Q

What characterises allergic tissue reactions in atopic subjects?

A

Infiltration of Th2 cells and eosinophils

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8
Q

How do IgE cause acute/chronic symptoms of allergy?

A

1)Allergen binds to IgE-coated mast cell, mast cell degranulates and releases histamine, which causes the acute symptoms of allergy. 2)Memory cells become activated, with other mediators being released like Th2 cytokines and chemokines, this produces the chronic symptoms of allergy

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9
Q

What are the interleukins released from Th2 cells that produce allergic inflammation?

A

IL-4 -> IgE synthesis. IL-5 -> Eosinophil development. IL-9 -> mast cell development. IL-13 -> IgE synthesis, airway hyperresponsiveness and goblet cell hyperplasia

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10
Q

What is allergic rhinitis?

A

Allergy to enzymes in pollen grains -> enzymes leach out when the pollen grains land on eyes or nose, which causes IgE response

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11
Q

How does allergic rhinitis affect the popn?

A

Affects 12-15% of children, 11-17% of adults, with effect on school exams

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12
Q

What causes Seasonal allergic conjunctive-rhinitis?

A

Mid-May to mid-Aug -> grass pollen. Apr to Mid-June -> tree pollen

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13
Q

What are the common causes of perennial allergic rhinitis?

A

House dust mite, cats, dogs, horses, cockroach, alternaria (fungal mould)

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14
Q

What is asthma?

A

Airways get narrow because of inflammation; noarrowing due to constriction of smooth muscle, oedema in airways and plugging of small airways

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15
Q

What are the symptoms of asthma?

A

Cough, shortness of breath, wheezing, chest tightness, secretions

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16
Q

What are the different phenotypes of asthma and do they cause allergy?

A

Early-onset allergic -> Th2 so often allergic. Late-onset allergic -> Il-5 so less allergic. Not allergic: exercise-induced (Th2), obesity-related (no Th2 markers), neutrophilic (Th17/IL-8)

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17
Q

What are the anaphylaxis symptoms?

A

Dizziness, seizures, loss of conciousness, lip, tongue swelling, laryngeal oedema, bronchoconstriction, arrhythmia, V/D pain, tingling, hives

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18
Q

What are some causes of anaphylaxis?

A

Drugs (penicillin), foods (peanuts, tree nuts, milk, eggs, fish, shellfish, sesame seeds, soy beans, celery, celeriac), insect stings (bees, wasps, hornets), latex

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19
Q

What treatment is used for anaphylactic shock?

A

Adrenaline

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20
Q

What are some examples and their causes of extrinsic allergic alveolitis?

A
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21
Q

How does extrinsic allergic alveolitis mechanism work?

A

Spores are inhaled, Ag/Ab complex formed in the interstitium, which then becomes inflammed, oedematous and gas exchange is impaired

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22
Q

What is the hygiene hypothesis?

A

Loss of species diversity, origins in sanitation rather than hygiene -> doesn’t involve personal hygeine

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23
Q

What are the factors associated with allergy/asthma prevalence?

A
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24
Q

How do dendritic cells become involved in allergy?

A

Lactobacilli (fermented food), saprophytic mycobacteria (dirt), helminths all help boost Th0 to become Treg cells, so have a protective function. However, with change in lifestyle, such as not playing in the dirt, less fermented food, there is more tendency for Th0 to become Th1/2

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25
Q

What are the 3 main methods of allergen disease treatment?

A

Allergen avoidance, anti-allergen medication, immunotherapy (desensitisation/hyposensitisation)

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26
Q

What are some anti-allergen medication?

A

Anti-histamines, bronchodilators and corticosteroids

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27
Q

What is the method of allergen-injection immunotherapy?

A

Subcutaneous Immunotherapy: Beginning with small amounts and then building up to large amounts of the allergen, given subcutaneously over a very long period of time, leads to amelioration of the symptoms. Sublingual immunotherapy: same but given under the tongue, as SCIT could lead to severe anyphalactic shock

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28
Q

What are the advantages and disadvantages of allergen-injection immunotherapy?

A

Adv: effective and produces long lasting immunity. Disadv: Occasional severe allergic reaction, time consuming, standardisation problems

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29
Q

What are indications for allergen-specific immunotherapy in the UK?

A

Grass and tree pollen allergic rhino-conjuctivitis uncontrolled by medication. Bee or wasp sting anaphylaxis at risk for repeated stings

30
Q

How does allergen-specific immunotherapy work?

A

Down regulation of Th2, up-regulation of Th1 and Treg

31
Q

What is hypoxia?

A

Specific environment where the PO2 is low

32
Q

What is hypoxaemia?

A

Blood environment where PaO2 is low

33
Q

What is ischaemia?

A

Tissues receive inadequate oxygen

34
Q

What factors can put the body under hypoxic stress?

A

Altitude, exercise (but mechanism is very good), disease (COPD)

35
Q

How is oxygen transported across the body?

A

Air moves into the lungs, after being humidified and then moves from the conducting airways to respiratory airways, where it mixes with gases that are already there -> then it diffuses across into the capillary (which arrives with 75% saturation) and is then fully oxygenated -> before returning to the heart, the bronchial veins drain into the pulmonary veins and return to the heart (decreases Saturation to 97%

36
Q

What is the oxygen cascade?

A

Decreasing O2 tension from inspired air to respiring cells -> Fick’s law of diffusion states that flow rate is proportional to the pressure gradient -> inspiring hypoxic gas reduces the pressure gradient

37
Q

How is Fick’s law affected by different diseases?

A

Strucutural diseases reduce area, Fluid in alveolar sacks increases thickness and inspiring hypoxic gas reduces the pressure gradient

38
Q

What causes the O2 dissociation curve to shift right?

A

Increased metabolism: increased acidity, hypercapnia, increased 2,3-DPG concentration

39
Q

What causes the O2 dissociation curve to shift left?

A

Decreased acidity, hypocapnia, decreased 2,3-DPG concentration

40
Q

What does polycythaemia and anaemia do to the O2 dissociation curve?

A

Polycythaemia shifts curve up as there is more Hb present for binding. Anaemia shifts the curve down, as there is less Hb available for binding

41
Q

What is the amount of diffusible gas proportional to?

A

SA for gas exchange, diffusion constant and diffusion gradient

42
Q

Describe the oxygen cascade:

A

Start with 21.3kPa of O2, which is humidified (a bit of O2 lost) -> as you go further down the airways, mixing of old and new air occurs (bar can be moved up/down due to hyper/hypoventilation. No change between alveoli and alveolar capillaries but slight decrease in post-alveolar arteries due to bronchial drainage

43
Q

How is O2 transported?

A

2% dissolved and 98% bound to Hb

44
Q

What can affect the O2 cascade?

A

Alveolar ventilation, Ventilation/Perfusion matching, diffusion capacity and cardiac output

45
Q

How does ventilation/Perfusion matching affect the oxygen cascade?

A

Ventilating not/hyperperfused airways or perfusing non-ventialted airways means efficient gas exchange is not achieved

46
Q

How does diffusion capacity affect O2 cascade?

A

Some diseases can affect the parenchyma to become thickened and less conducive to exchange

47
Q

How does Cardiac output affect O2 cascade?

A

Increasing CO increases blood flowing through the lungs, so increasing O2 delivery

48
Q

How is gas transport changed during exercise?

A

When exercise is started, proprioreceptive afferent fibres from the muscles send signals to the medulla to increase the breathing -> also motorcortex before contracting the muscle sends a signal to the medulla to increase breathing -> then body fine tunes it until you reach a good supply/demand ratio -> once you finish the neurological stimuli are removed very quickly, but after exercise you tend to overbreath, trying to repay the O2 debt

49
Q

What is the ventilatory response to exercise?

A

Tidal volume increases early; resp frequency stabilises at 20 breathspm and increases later, when you reach the upper thresholds of exercise

50
Q

What does the hypoxic oxygen cascade look like?

A

Such as at Mt Everest -> barometric hypoxia

51
Q

What are the five challenges of altitude?

A

Hypoxia -> much less O2 in ambient air. Thermal stress -> freezing cold weather, high wind-chill factor. Solar radiation -> less atmospheric screening, reflection of snow. Hydration -> water lost humidifying inspired air, hypoxia induced diuresis. Dangerous -> windy, unstable terrain, hypoxia-induced confusion and malcoordination

52
Q

How does accommodation occur during hypoxia?

A

As decrease in CO2 isn’t the issue for over-breathing, you dig into a hole, where the central control says to breathe less, and the sympathetic outflow says breath more. Kidneys help correct the pH by increasing the amount of HCO3- excreted. Anaerobic metabolism should be avoided

53
Q

What is acclimation?

A

Stimulated by an artificial environment -> like acclimatisation (hypobaric chamber or breathing hypoxic gas)

54
Q

How can you prevent prophylaxis due to hypoxia?

A

Acclimation and acetazolamide (carbonic anhydrase inhibitor, accelerating the renal compensation to hypoxia-induced hyperventilation)

55
Q

What are some innate/developmental adaptations for hypoxic environments?

A

Barrel chest -> larger TLC, more alveoli and greater capillarisation. Increased haematocrit -> greater O2-carrying capacity of the blood. Larger heart -> to pump through vasoconstricted pulm circulation. Increased mitochondrial density -> greater O2 utilisation at cellular level

56
Q

What is chronic mountain sickness?

A

Secondary polycythaemia increases blood viscosity which sludges through systemic capillary beds impeding O2 delivery

57
Q

What are the causes, symptoms and consequences of chronic mountain sickness?

A

No known cause; symptoms: cyanosis, fatigue. Consequences are ischemic tissue damage, heart failure and eventual death

58
Q

How can chronic mountain sickness be treated?

A

No interventional medical treatment -> sufferers exiled to lower altitudes

59
Q

What is Acute mountain sickness?

A

Associated with mild cerebral oedema, nausea, vomiting, irritability, dizziness, insomnia, fatigue, dyspnoea

60
Q

What are the causes, treatment and consequences of acute mountain sickness?

A

Causes: maladaptation to high-altitude environment -> usually associated with recent ascent, w/in 24h and can last more than a week. Consequences: Development in to HAPE/HACE. Treatment: monitor symptoms, stop ascent, analgesia, fluids, medication or hyperbaric O2 therapy, with symptoms subsiding after 48h of increased renal compensation

61
Q

What is HACE?

A

High-altitude cerebral oedema -> vasodilation of vessels in response to hypoxaemia, more blood going into capillaries increases fluid leakage -> cranium is a sealed box so intracranial pressure increases

62
Q

What are the causes, symptoms and consequences of HACE?

A

Causes: Rapid ascent/inability to acclimatise. Symptoms: confusion, ataxia, behavioural change, hallucinations, disorientation. Consequences: irrational behaviour, irreversible neurological damage, coma, death

63
Q

What is the treatment for HACE?

A

Immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone

64
Q

What is HAPE?

A

High altitude pulmonary oedema -> vasoconstriction of pulm vessels in response to hypoxia; increased pulm pressure, permeability and fluid leakage from capillaries; fluid accumulates once production exceeds the maximum rate of lymph drainage

65
Q

What are the causes, symptoms and consequences of chronic mountain sickness?

A

Causes: Rapid ascent or inability to acclimatise. Symptoms: Dyspnoea, dry cough, bloody sputum, crackling chest sounds. Consequences: impaired gas exchange, impaired ventilatory mechanics

66
Q

What is the treatment for HAPE?

A

Descent, hyperbaric O2 therapy, nifedipine, salmeterol, sildenafil

67
Q

What is type I respiratory failure?

A

Fundamentally failure of pulm gas exchange, generally V/Q inequality, MAINLY O2 (because CO2 can diffuse easily) -> hypoventilation, V/Q mismatch, diffusion abnormality

68
Q

What can cause Type I Respiratory failure?

A

Pulmonary oedema, pneumonia, atelactasis

69
Q

What are the different types of respiratory failure?

A

T1 - hypoxic -PaO2 6.7kPa

70
Q

What causes T2 RF?

A

Increased CO2 production, decreased CO2 elimination -> decreased CNS drive, increased work of breathing, pulmonary fibrosis, neuromuscular disease, increased physiological dead space, obesity

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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