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PoM - Principles of Medicine Week 2 > Anaphylaxis > Flashcards

Anaphylaxis Flashcards

1
Q

What type of hypersensitivity is anaphylaxis?

A

Acute Type 1 - results from an IgE-mediated response to an allergen, can be systemic

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2
Q

Why does our body have immunity?

A

To protect against foreign antigens only (generally cannot identify if molecules are harmful or not, just whether they are self or non-self)
Non-self / foreign antigens trigger immune response

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3
Q

What are the 2 types of immunity and what are their features?

A

Innate and adaptive -
Innate = ability to recognise material that should not be present in the body from very blunt structural features e.g. bacterial protein, first amino acid is fmet unlike for mammals, met. The innate system can recognise this as they have a receptor site for fmet
e.g. viral infections, system detects large amounts of double stranded RNA, which is not present in mammals. It is non-specific as it does not need to know what type of virus it is
Causes immune system to fire off and initiates the adaptive immune system
Adaptive = Specific response that generates antibodies (Abs) and long term immunity by the production of memory cells
Abs have specific structures to bind / complement specific antigens
Takes some time to develop

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4
Q

What is the adaptive immune system used for medically?

A

Vaccines - trigger immune response, so if same pathogen encountered again, the adaptive immune system can rapidly produce many Abs to defend before it can cause harm

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5
Q

Innate vs adaptive (define using an adjective)

A

Innate - non specific

Adaptive - specific

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6
Q

What is an antigen?

A

Protein marker on cell surface that triggers an immune response

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7
Q

What causes the interaction between the antigen and antibody?

A

Shape and charges
Interaction is driven by a mixture of shape (i.e. antigen complementary to the variable site on the Ab) and charge (positive and negative charges attract)
Overall - complementary shape and distribution of charge

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8
Q

What is the biggest issue for the adaptive immune response?

A

Auto immune conditions can develop (chronic)
Must not recognise self cells, because if it does it will destroy own body tissue causing inflammation and tissue damage
E.g. type 1 diabetes, lupus, rheumatoid arthritis

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9
Q

What is an antibody (Ab)?

A

A specific protein that can bind to an antigen using charges and shape (must be complementary to the antigen)

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10
Q

What are the symptoms of anaphylaxis?

A

Skin feeling hot, redness
Itchiness
Puffing up
Chest feels tight

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11
Q

Why does the skin feel hot, red, and itchy during an anaphylactic attack?

A

Vasodilation

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12
Q

Why does the skin and body swell / puff up during an anaphylactic attack?

A

Caused not by red cells, but just fluid build-up e.g. water and proteins due to lost membrane / osmotic integrity
Tight junctions between endothelial cells in the blood vessels get looser due to the release of histamine from basophils / mast cells, so fluid gets through into tissue, oedema (fluid from blood builds up in tissues)

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13
Q

How does vasodilation work?

A

Signalling between endothelium and smc
In vasculature, histamine reaches endo thelial first - causes endo to contract a tiny bit and makes nitric oxide - causes smc to relax

Tight junctions between endo looser, fluid gets through into tissue, oedema ( fluid from blood build up in tissues)

HOWEVER, in bronchi, histamine released by basophil causes contraction ?

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14
Q

What are the structures of the blood vessel and the bronchus?

A

Both have a similar structure:
2 layers around: inner layer of endothelial cells
Outer layer of smooth muscle cells
(And elastic membranes)

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15
Q

What happens to the smooth muscle during bronchoconstriction and why?

A

Normally smooth muscle cells are relaxed to open brochus airway (dilated), however, during bronchoconstriction the smooth muscle cells contract

This is because mast cell and basophils release histamine during an immune response to cause dilation of blood vessels - in the bronchus, however, this release of histamine causes contraction of smooth muscles leading to bronchoconstriction

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15
Q

Korbv knprfomprf

A

Efuvfriv metopes

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16
Q

How does vasodilation work?

A

Process involves signalling between endothelium and smooth muscle cells
Mast cells and basophils release histamine
In vasculature, histamine reaches the endothelial first, causes the endothelial cells to contract a little but predominantly causes it to make and release nitric oxide. NO causes the smooth muscle cells to relax, therefore leading to vasodilation

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17
Q

What effects does the release of adrenaline have on the body?

A

Increases heart rate
Redirects blood away from the skin and towards the vital organs
Bronchodilation
Peripheral vasodilation (can help reverse puffiness)
Increases BP

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19
Q

What causes patients to faint / pass out during an anaphylactic attack?

A

The combination of vasodilation and a leaky endothelium that lets blood out causes BP to drop
Not enough blood is pumped to the brain and other vital organs

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20
Q

What is the role of IgE during an anaphylactic reaction?

A

IgE - sits on Fc receptor on mast cell triggering it to release histamine

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21
Q

What may cause the abrupt change for the patient to suddenly become allergic to something they were not to before?
e.g. for this patient who was involved in a traumatic car accident and was administered penicillin by IV as a part of his treatment

A

Patient most likely did have Abs against penicillin from before, but not IgE Abs
Developed after due to the combination of stress (from trauma) and the large dose of penicillin
Sensitisation to penicillin as it was administered by IV, so probably lead to a much bigger dose
Genetics can also make you susceptible to this change (As well as the stress and dosage)

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22
Q

What determines the class of an Ab, and what is the significance of different classes of Abs?

A 
Classic Ab has light and heavy chains
Heavy chains determine the class of Ab - IgA, IgG, IgE or IgM
The class of the Ab determines the next step in the immune response
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23
Q

What class of Ab is the first Ab made when interacting with a foreign antigen?

A

IgM (light chains selected during immune response)

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24
Q

What is the life cycle of an antibody (Ab)?

A

As a foetus/baby, the body makes every possible combination and then identifies the ones that are self-recognising antigens. These are then destroyed
Exons can be used to make the variable region in the light chain e.g. specific amino acid sequences selected from different sections of exons to make new variable regions

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25
Q

How to make a heavy chain for IgE?

A

The DNA sequence for the IgM antibody involves : Promoter, IgM sequence, delta … (many more), IgE sequence, then stop region

By cutting out all the DNA between the promoter and the IgE sequence during the process of rearrangement to make specific Abs, IgE Ab is formed

26
Q

Why did IgE Abs evolve?

A

For helminths (worms)

27
Q

What triggers the class switch response?

A

Genetics - more likely to make the switch

Combination of stress and dose

28
Q

What treatment is given to someone with an anaphylactic reaction?

A

Epinephrine / adrenaline
Oxygen
IV anti-histamines
IV corticosteroids - i.e. other anti-inflammatories
Lay down patient with feet raised (increased blood supply to brain - gain consciousness)

29
Q

What triggers a fight or flight response and what occurs during it?

A

Produced when scared or angry - adrenaline released
Prioritises heart, legs, lungs and brain by directing blood flow towards those areas during a stressful situation
Affects leave quickly after escape from danger

30
Q

Why does the effect of adrenaline leave quickly and what occurs during chronic stress?

A

Adrenaline has a short half life

Chronic stress is a result of continuous production of adrenaline (not an increased half life of adrenaline)

31
Q

Why keep him overnight to monitor him?

A

Normally penicillin would have a short half life if we had enzymes against it (but we do not)
Monitored to maintain his BP, see if antihistamines have had their effect

32
Q

What class of Ab is normally floating around in the blood and how can this eventually lead to the production of IgE?

A

IgG

33
Q

How does the body produce a specific Ab to an antigen?

A

First make an Ab to the antigen that complements it reasonable well
Then cause hyper mutations in the gene that codes for that Ab
Eventually, a more specific binding site is created from the new mutations, which results in a better fit to the antigen

34
Q

What type of cell causes these symptoms?

A

Mast cells (and basophils)

35
Q

What is the signalling molecule involved?

A

Histamines

36
Q

What Ig class is likely to be involved?

A

IgE

37
Q

What causes redness / rashes / puffy skin?

A

Vasodilation of the blood vessels

38
Q

Why should adrenaline be given?

A

Counters the effects of histamine (e.g. vasoconstriction, blood flow to vital organs)

39
Q

What sorts of drugs might have been in subsequent injections?

A

Steroids (if it doesn’t settle down)
Different antibiotics
Antihistamines
Oxygen mask

40
Q

Why did the patient faint?

A

Low BP

41
Q

Why was the BP monitored in the hospital overnight?

A

Good indicator of what’s going on behind the scenes - if it going up then you know the heart is doing well

42
Q

What is anaphylaxis?

A

Acute type I hypersensitivity reaction
Can be systemic
IgE-mediated response to an allergen

43
Q

What is the normal pathway of lymphocyte activation?

A

Antigen binds to surface IgM found on lymphocytes
This stimulates proliferation and secretion of Abs
Usually, the Ab initially secreted is IgM, and this switches to IgG as the immune response progresses

44
Q

What occurs during type 1 hypersensitivity that produces IgE?

A

Activation of CD4+ T helper cells (Th2) causes a switch to IgE production
IgE binds to IgE-receptors on the surface of mast cells
Several IgE will bind to the FCeR1 (which have a high affinity for IgE) on the mast cells
Subsequent stimulation of these cells by exposure to the antigen causes the mast cells to degranulate

45
Q

What is the name given to the antigens that cause allergies?

A

Allergens

46
Q

Where can mast cells be found and what are their features?

A

Widely distributed throughout the body in connective tissue (e.g. under the skin) and in association with epithelial mucosae (e.g. the respiratory and intestinal epithelia)
Contain granules of inflammatory mediators - most notably histamine and leukotrienes

47
Q

What occurs to mast cells when antigens bind to surface IgE?

A

Inflammatory mediators are released

48
Q

What do the Inflammatory mediators act on?

A

Principally, on blood vessels and smooth muscle

49
Q

What are the effects of histamines?

A

Vasodilation -
Increased movement of fluid out of blood - oedema
(Oedema around the larynx can contribute to dyspnoea - difficulty breathing)
Bronchoconstriction -
Causes shortness of breath
Loss of blood volume (due to extravasation of fluid) leads to hypotension (low BP)
Heart rate increases slightly but the force of contraction decreases
Contraction of smooth muscle in the walls of the intestines

50
Q

What are the features and causes of a skin allergy?

A

Redness and puffiness / rashes - sure to stimulation of connective tissue mast cells which cause vasodilation

51
Q

What is this type of rash in response to a skin allergy called?

A

Urticaria

52
Q

What does allergy testing involve?

A

Localised skin reaction by injecting small amounts of possible allergens using a pin prick
Looks for a localised wheal-and-flare reaction

53
Q

Common allergens of skin allergies?

A

Animal hair
Proteins in natural latex
Certain chemicals
Substances in insect and plant stings

54
Q

What happens when the allergen is inhaled?

A

Principal site of action will be mucosal mast cells of the respiratory system
Allergic rhinitis (i.e. during hay fever) - if the allergen is in the nasal passage, oedema in the epithelia lining the nose leads to general irritation including stimulation of mucus secretion
If the allergen reaches the bronchioles of the lungs, you get contraction of smooth muscle - decreases the diameter of the airways and causes inflammation and increased mucus production. Results in asthma - difficulty breathing in and especially breathing out

55
Q

What happens if the allergen is ingested? (i.e. in food allergies)

A

Will act at the mucosal mast cells in the intestinal tract
Stimulation of associated smooth muscle leads to vomiting and diarrhoea - typical of food allergy
If the allergic substance can be absorbed and pass into the blood stream, it may also cause skin symptoms (rashes or itching)

56
Q

What are common symptoms of an anaphylactic attack?

A

Dilation of peripheral blood vessels causes rashes and oedema
Results in dramatic drop in blood pressure - affects organ function, this is shock
Bronchoconstriction causes difficulty in breathing
nausea, abdominal cramps or diarrhoea (from effects on the intestines)

57
Q

What is the patient’s response to an anaphylactic attack?

A

Increase respiratory and heart rate

58
Q

How are anaphylactic attacks treated medically?

A

Treated as a medical emergency - could be fatal
Emergency treatment is aimed initially at the hypotension and then the underlying inflammation
Patient is laid down with feet raised in order to improve blood supply to the head and trunk
Injection of adrenaline to constrict peripheral blood vessels and redirect blood to the organs
IV drip may be used to control blood pressure
antihistamines and anti-inflammatory corticosteroids (to help control allergic response)
If breathing problems persist, oxygen and bronchodilators

59
Q

What is the feature of substances that can cause anaphylaxis in susceptible patients and some examples?

A

Substances that can pass freely around the body - e.g.
Penicillin
Some other drugs (e.g. local anaesthetics, X-ray contrast agents)
Venom in bee or wasp stings
Peanuts (allergen can be absorbed fast enough to cause systemic effects)

60
Q

What is the long term treatment for anaphylaxis?

A

Avoid known allergens

For patients who cannot completely avoid the allergen, medications, epipens (for self-injection of adrenaline)

PoM - Principles of Medicine Week 2 (12 decks)

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