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JMP Y2S1 > Week 33- Skin and Allergy > Flashcards

Week 33- Skin and Allergy Flashcards

1
Q

What is an allergic reaction?

A

It is a hypersensitivity reaction to “harmless” environmental factors (allergens = antigens)

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2
Q

How common is allergic disease within the Australian population?

A

20% has allergic disease

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3
Q

What are common reactions to allergic disease?

A

Itch
Runny nose
Rashes
Sneezing

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4
Q

What is a severe reaction during allergic disease?

A

Anaphylaxis

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5
Q

What are examples of allergen categories?

A 
Food allergens (wheat, dairy products)
Inhaled allergens (house dust-mite, pollens)
Medications (penicillin)
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6
Q

What determines the response of an allergy?

A

Determined by the route of exposure and the immune response activated

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7
Q

What are some sites of allergen exposure?

A

Skin
Injection
Ingestion
Inhalation

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8
Q

What is the mechanism of allergic immune activation?

A
  1. Allergen exposure to epithelium causes cytokine release (IL-25, IL-33, TSLP)
    1. Activation of ILC2s
    2. Activation of local antigen presenting cells (APCs)
    3. T cell activation –> TH2 cells generated in presence of IL-4
    4. B-cell activation –> IgE produced in presence of IL-4/TH2
    5. Mast cell activation by IgE –> release histamine
    6. Eosinophil activation by IL-5
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9
Q

What is the early phase of allergic response?

A

In pre-sensitised individuals:

Early response –> Mast cell activation and release of granular molecules

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10
Q

What is the late-phase response in allergic response?

A

Activation of APC and TH2 cells
T-cell proliferation
Activation of eosinophils

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11
Q

What does a Type I hypersensitivity reaction require?

A

Prior exposure and immune sensitisation –> to produce IgE antibody

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12
Q

What is the time of appearance and immune mechanism behind Type I hypersensitivity?

A

Time = 2-30minutes (very fast) (requires previous exposure)
Allergen binds to IgE antibodies on mast cell surfaces (acute inflammatory response) –> mast cells degranulate and release immune mediators (histamine etc)
E.G = allergic asthma, allergic rhinitis, eczema

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13
Q

What is the time of appearance and immune mechanism behind Type II hypersensitivity?

A 
Time = 5 - 8 hours
Mechanism = Humeral IgG binding to cellular antigens (allergen) leads to damage of self cells --> Antibody and complement (cytotoxic result)
E.G = some drug allergies eg penicillin
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14
Q

What is the time of appearance and immune mechanism behind Type III hypersensitivity?

A 
Time = 2-8 hours
Mechanism =  Humeral IgG binds to blood-borne allergen (forms insoluble complex)Complement pathways lead to tissue damage in sites of complex deposition.
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15
Q

What is the time of appearance and the immune mechanism behind type IV hypersensitivity?

A

Time = 24-72 hours (delayed response)
Mechanism = Immune cell mediated response (T cell) (can be granulonatous) –> no antibody involvement
E.G –> response to large insoluble antigens, contact dermatitis, chronic asthma, graft rejection

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16
Q

Does drug allergy relate to the toxicity or side effects of a drug?

A

No, it cannot be predicted pharmacologically

No link between dose and response

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17
Q

What are some common symptoms of drug allergies?

A
  1. Skin rash/hives
  2. Itching
  3. Wheezing/ breathing problems
  4. Muscle and joint pain
  5. Swelling/angioedema –> facial swelling typically
  6. Anaphylaxis
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18
Q

What is anaphylaxis?

A

Severe, life threatening allergic reaction

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19
Q

What are common drugs that can trigger an allergic reaction?

A
  1. Chemotherapy
    1. Antibiotics containing sulphonamides
    2. Aspirin, ibuprofen and other NSAIDS
    3. Anticonvulsants
    4. Penicillin and related antibiotics
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20
Q

How does the direct presentation mechanism of drug allergy work?

A
  1. Drugs are too small to activate the adaptive immune system
    1. Drugs first can interact with the MHC-peptide complexes on the antigen presenting cells —> interaction can change the normal non reacting self peptides to a reactive structure
    2. T cells screen for their TCR recognition
    3. TCR binds to the altered MHC region and activates a T cell response against the drug
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21
Q

What is the Hapten mechanism of drug allergy?

A
  1. Drug molecules or metabolites can act as Haptens
  2. Happens are drugs that irreversibly binds to carrier proteins which are then displayed in the MHC (this mechanism happens in penicillin)
  3. Adaptive immune response is then initiated through T cell recognition of the drug protein complex
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22
Q

What is the difference between a Hapten and a pro-Hapten?

A
  1. Hapten is a drug that irreversibly binds to a carrier protein
    1. Pro-Haptens are inert drugs that are processed into reactive metabolites which can act as Haptens.
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23
Q

What hypersensitivity reactions can be caused by drug allergy?

A

All of them

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24
Q

How is a drug allergy diagnosed?

A
  1. Skin test

2. Drug challenge –> under carefully controlled conditions

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25
Q

How are drug allergies treated?

A
  1. Avoidance where possible
  2. Antihistamine treatment
  3. Bronco dilators, adrenaline and oxygen to help deal with respiratory distress
  4. Desensitisation if possible
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26
Q 
What are the three types of adverse drug reactions for eg penicillin?
For:
common
infrequent
True anaphylaxis
A
  1. Common adverse drug reactions —> eg diarrhoea, nausea, rash
    1. Infrequent adverse effects —> eg fever, vomiting, erythema dermatitis, angiodema (swelling), seizures.
    2. True anaphylaxis (drug allergy) —> eg hypotension, angiodema, broncospasm.
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27
Q

What are cytokines?

A

Signalling molecules that orchestrate inflammatory response and ramp up the immune systems response to pathogens.

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28
Q

What are some ways cytokines ramp up the immune response?

A
  1. Activates cells of the immune system
    1. Acts on blood vessels to allow proteins, fluid and cellular blood elements to leave the circulation and get to the affected tissue
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29
Q

What happens to cytokines numbers when the amount of pathogen decreases?

A

They decrease as the level of secreted cytokines reduces —> the response subsides.

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30
Q

What happens when there is no subsiding of cytokines?

A

Cytokines storm —> uncontrolled inflammation within tissue and key organs

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31
Q

What are some key cytokines in allergic response?

A

IL-4 –> released by TH2 to stimulate clonal expansion
IL-4 and IL13 –> drive B-cell antibody production
In asthma –> IL3,4,9,13 important

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32
Q

What are some certain infection types that increase the risk of cytokine storm?

A
  1. systemic infection
    1. septic shock
    2. SARS
    3. bird flu (H5N1)
    4. Hanta virus infection
    5. Ebola
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33
Q

How is atopic (allergenic) asthma induced?

A

Allergen induced activation of submucosal mast cells leading to TH2 mediated chronic inflammation

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34
Q

After initial exposure is the presence of the allergen required to give an effect in chronic atopic asthma?

A

Not necessarily as the response may be perpetuated even in the absence of the allergen and can be triggered by other factors as well.

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35
Q

What are the 4 clinical levels of asthma and what is the difference in each?

A

Step 1 —> less than once a week and brief symptoms
Step 2 —> more than once a week but less than once every day
Step 3 —> daily FEV1 between 80 and 60% predicted
Step 4 —>daily, loss of ability for physical activity FEV1 less than 60% predicted

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36
Q

Are x-rays useful in people with asthma?

A

Not really in 75% of cases x-rays appear normal

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37
Q

What are some X-ray features that may be present in asthmatics?

A
  1. Pulmonary hyperinflation
    1. Bronchial wall thickening
    2. Pulmonary wall oedema
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38
Q

What are some factors that contribute to virus induced wheezing illness?

A
  1. Genetics —> history of asthma or atopy, poor antiviral immunity, risk genes and SNP
  2. Preexisting airway inflammation —> TH2 polarised inflammation, airway damage/remodelling
  3. Virus infection —> Rhinovirus A and C, Respiratory syncytial virus
  4. Treatment —> corticosteroid use, monoclonal antibody use for virus treatment
  5. Environment —> exposure to allergens —> smoke, tobacco, pollen
  6. Microbiome —> loss of diversity
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39
Q

What are some clinical features of Atopic dermatitis?

A

Onset is 3-6months of age
May appear in childhood or adolescence but normally clears by the age of 2
Persistence into later life is normally frequent cycles of remission and exacerbation.

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40
Q

What are the signs of atopic dermatitis?

A

Dry and scaly skin
Active lesions intensely pruritic (itchy)
Chronic lesions thickened and lichenified
Commonly accompanied by atopic respiratory allergy
Symptoms commonly independent of allergen exposure
Very high IgE possible

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41
Q

What is the pathology of atopic dermatitis?

A

Mononuclear cell infiltration and CD4 cells

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42
Q

What is the common bacteria or virus for atopic dermatitis?

A

Rarely viral

Commonly staph aureus Or strep pyrogenes

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43
Q

How common are auto immune diseases and which gender is impacted more?

A

5-10% of the population with 2/3 of cases being in females

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44
Q

Is B or T cell tolerance more important to avoid autoimmunity?

A

T-cell tolerance

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45
Q

What are some thymic tolerances to reduce autoimmunity?

A
  1. +/- selection leading to deletion

2. Weakly self reacting lymphocytes rendered unresponsive (anergy)

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46
Q

What are some peripheral tolerances to reduce autoimmunity?

A
  1. Ignorance (self antigens are invisible)
    1. Separation of autoreactive T cells and Ag
    2. Anergy and lack of self stimulation
    3. Suppression induced by regulatory T reg cells
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47
Q

What is anergy?

A

absence of the normal immune response to a particular antigen or allergen.

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48
Q

What is the causative agent in Hep B?

A

DNA virus

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49
Q

What is poly arthritis nodosa (PAN)?

A

It is a necrotising vasculitis of medium sized muscular arteries.

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50
Q

How does PAN relate to Hep B?

A

It is mostly observed in patients with Hepatitis B
It is caused by circulating immune complexes
Immunoglobulin and complement deposit on the walls of the involved vessels and cause vascular infiltration of neutrophils and mononuclear cells.

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51
Q

How does poly arthritis nodosa normally present?

A 
Myalgia --> muscle pain
Arthralgia --> joint pain
Fever
Weight loss
Multisystem disorders --> reflective multiorgan involvement
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52
Q

How is PAN treated?

A

Removal of hepatitis B antigens (antiviral therapy)

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53
Q

What is the causative agent of Hepatitis C?

A

RNA virus

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54
Q

What is cryoglobinaemic vasculitis?

A

Palpable purpura (rash of purple spots due to small blood vessels leaking blood into skin) over lower extremities, arthralgia (joint pain) and neuropathy.

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55
Q

How does cryoglobinaemic vasculitis involve Hep C?

A

Molecular mimicry HCV E2 protein is antigenically similar to human Igs and this stimulates anti Ig antibodies that can in turn stimulate the complement cascade, forming immune complex that deposit in vessels.

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56
Q

What are the Cryoglobin molecules formed by?

A

The Cryoglobulin (CG) molecules formed are of a mixture of polyclonal IgG and monoclonal Igs usually of IgM type CG deposit in blood vessels

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57
Q

What are the two infection types in HIV?

A

HIV1 and HIV2

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58
Q

What are the key differences between HIV1 and HIV2?

A

HIV 1 —> worldwide, higher mother-offspring infection rate, 7-10years till AIDS
HIV 2 —> west Africa, lower mother-offspring infection rate, 10-25 years till AIDS

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59
Q

How does HIV infection start and progress?

A
  1. Primary infection asymptomatic/ influenza like
  2. Acute viremia is followed by antibody production (seroconversion)
  3. Period of clinical latency (2-15 years)
  4. HIV virus is an envelope RNA virus (retrovirus) enters cells by means of gp120 binding to CD4 (on T cells. DC and Mf) and co-receptors CCR5 (DC, Mf) or CXCR4 (T cells)
  5. Antibodies and CD8 cytotoxic responses directed against the HIV remain high during the asymptomatic phase
  6. Following progressive loss of CD4 T cells there is increase in HIV number and decrease in antibody and CTL responses leading to opportunistic infections and malignancies(due to immunodeficiency)
  7. Causes immune dysregulation –hypergammaglobulinaemia and autoimmune diseases
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60
Q

What are some HIV driven autoimmune complications?

A
  1. HIV associated Immune Thrombocytopenic Purpura (ITP)
    • In 5-30% of pts with HIV and may be the 1 st manifestation
    • Treatment strategies: steroids, IV immunoglobulins, plasmapheresis, interferon-alpha therapy, splenectomy with retroviral therapy
  2. Autoimmune Haemolytic Anemia in HIV (AHA)
    • AHA is very rare in pts with HIV Usually occurs in very advanced stages
    • Direct antiglobulin test can sometimes give false positive results
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61
Q

What are the two mechanisms by which HIV drives Thrombocytopenic purpura (ITP)?

A

Mechanism 1: Peripheral platelet destruction with anti-GpIIIa antibodies & activation of immune complexes
Mechanism II: defect in platelet production due to infection of megakaryocytes

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62
Q

What is Guillain-Barre Syndrome (GBS)?

A

An acute inflammatory or post-infective demyelinating polyneuropathy:

  • 70% history of respiratory infection of diarrhoea 1-4 weeks pre onset
  • Some cases occur following surgery or post immunisation
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63
Q

Symptoms of GBS?

A
  1. Weakness in legs
    1. “Pins and needles” feeling in extremities
    2. Difficulty with eye or facial movements
    3. Body aches
    4. Bowel or bladder issues
    5. Rapid heart rate
    6. Low/high BP
    7. Difficulty breathing
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64
Q

What is one of the major exposures that can lead to GBS Guillain barre syndrome?

A

Approximately 25-50% of patients with GBS have been exposed to Campylobacter jejuni

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65
Q

What virus’ have also been implicated GBS?

A

Viruses such as Epstein-virus, HIV, cytomegalovirus (Zika and chikungunya)

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66
Q

What is the immunological mechanism that leads to infection causing GBS?

A

Molecular mimicry

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67
Q

Why are nerve cells demyelinated in GBS?

A
  1. Antibody-mediated effector pathways, including complement activation, cause glial or axonal membrane injury with consequent conduction failure
  2. Acute inflammatory demyelinating polyneuropathy (demyelinating): molecular mimicry between glycans in LPS generating antibodies that bind to GM1 and GD1a gangliosides –leading to nerve conduction blockade
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68
Q

What is GAS?

A

Group A streptococcus pyogenes

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69
Q

What are some examples of superficial and deep tissue infections caused by GAS?

A
  1. Impetigo —> superficial —> minor trauma predisposes —> observed in children in hot an humid conditions —> superficial, intraepidermal, unilocular, vesicopustule
  2. Erysipelas —> superficial cellulitis —> occurs in areas of preexisting lymphatic obstruction or oedema —> painful lesions with bright red oedematous appearance
  3. Cellulitis and Fasciitis —> involve deeper structures —> requires immediate therapy/ surgery
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70
Q

What is Scarlett fever caused by?

A

Streptococcal pyrogenic Exotoxins

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71
Q

What are the symptoms of Scarlett fever?

A

Diffuse erythematous rash, blanching with pressure (7-10days)
Swollen tongue (strawberry)
Usually associated with GAS pharyngitis or tonsillitis

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72
Q

How does toxic shock syndrome cause death?

A

Cytokines storm and multi organ failure

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73
Q

How does streptococcal pyrogenic exotoxins cause toxic shock syndrome?

A

Act as super antigens –> massive T-cell stimulation –> cytokine storm and multiorgan failure

74
Q

What causes acute post-streptococcal Glomerulonephritis?

A

following infection with “nephritogenic strains” of Streptococci Involves immune complex deposition (type III hypersensitivity reaction)

75
Q

What is the standard clinical presentation of Acute poststreptococcal Glomerulonephritis?

A

Abrupt onset –> 1-4 weeks after GAS infection
Dark/smokey coloured urine
Recovery can take 10 years
2/3 of patient have complete recovery

76
Q

What triggers acute rheumatic fever and rheumatic heart disease? ARF/RHD?

A

triggered by GAS infection (unique to human)
Immune-mediated complication of GAS infection characterised by inflammation of the heart, joints, blood vessels and skin

77
Q

What regions are mainly affected by ARF/RHD?

A

Poor and developing regions

78
Q

What is the major virulence factor in ARF/RHD?

A

M protein —> inhibits phagocytosis, inhibits complement deposition, Binds host proteins, activates inflammation, adhesion, binds immunoglobulins

79
Q

What are the main factors we look at during physical examination of a skin lesion? (7)

A
  • Morphology
  • Size
  • Shape/configuration
  • Demarcation
  • Distribution
  • Colour
  • Consistency
80
Q

What is the main roles of skin?

A
  1. Temperature regulation
    1. Fluid regulation
    2. Vitamin D production
    3. First line in immune defence
81
Q

What are Macules?

A

non-palpable lesions ≤1 cm that vary in pigmentation from the surrounding skin (flat)

82
Q

What are Patches?

A

non-palpable lesions >1 cm.

83
Q

What are Papules?

A

palpable, discrete lesions measuring ≤1cm in diameter (isolated or grouped)

84
Q

What are Nodules?

A

palpable, discrete lesions measuring >1cm in diameter; tumours are large nodules.

85
Q

What are Plaques?

A

large (>1 cm) superficial slightly raised lesions, often formed by a confluence of papules.

86
Q

What are Purpura?

A

Red-purple lesions that do not blanch under pressure

87
Q

What are pustules?

A

Small skin papules containing purulent material

88
Q

What is Excoriation?

A

Superficial linear skin erosions caused by scratching

89
Q

What is Lichenification?

A

Increased skin markings and thickening –> secondary to chronic inflammation from scratching or irritation

90
Q

What is Scale?

A

Superficial epidermal cells which are dead and cast of the skin

91
Q

What is Crust?

A

Dried exudate

92
Q

What is a skin Fissure?

A

Deep skin split extending into the dermis, erosion is superficial, focal loss of part of the epidermis

93
Q

What is Ulceration?

A

Focal loss of the epidermis into the dermis

94
Q

What is Skin Atrophy denoted by?

A

Decreased skin thickness –> from skin thinning

95
Q

What is a Scar?

A

Abnormal fibrous tissue that replaces normal tissue after injury

96
Q

What is Hyper/Hypopigmentation?

A

Hyper –> increased skin pigment

Hypo –> decreased skin pigment

97
Q

What is the cause of skin scaling?

A

Parakeratosis

98
Q

What is the cause of erythema?

A

Dilation of skin vessels

99
Q

What is the physiological cause of blisters?

A

Separation of layers of the epidermis, or from a separation of the epidermis and dermis

100
Q

What is bruising caused by?

A

A leakage of blood into dermis

101
Q

What are some causes of skin pigmentation?

A
  1. Increased melanocyte activity
    1. Increased number of melanocytes
    2. Endogenous pigment eg ochronosis
    3. Endogenous pigment eg tattoo
102
Q

What is the physiological basis of skin plaques?

A

Increased in epidermal and dermal thickness with cells

103
Q

What is the physiological basis of macules?

A

Dilated blood vessels
Inflammatory cells
Altered pigmentation

104
Q

What is the physiological basis of papules?

A

Inflammatory cells
Oedema
Tumour

105
Q

What is the physiological basis of nodules?

A

Epidermal tumours
Aden always tumours
Dermal tumours
Cysts

106
Q

What is the physiological bases of rashes restricted to exposed area?

A

Photo sensitivity

Contact eczema

107
Q

What are some broad classifications of skin disorders?

A
  1. Skin infections —> bacterial, viral, fungal, parasitic
    1. Inflammatory skin conditions —> dermatitis, psoriasis, drug eruptions
    2. Skin cancers —> non melanomas (Basal, squamous cell carcinoma), malignant melanoma
108
Q

What is another name for atopic dermatitis?

A

Eczema

109
Q

What kind of inflammatory response is atopic dermatitis?

A

TH2 overactivity –> Humeral response antibodies –> B cells

110
Q

How can eczema/atopic dermatitis be characterised?

A
  1. Chronic conditions with “flare ups”

2. Pruritis (itching), dry skin, eczematous lesions, FHx of atopy

111
Q

How and when does eczema often present?

A

In children —> areas of skin thickening occurs in affected areas “lichenification”
Can also be as erythematous papules +/- ooze with crusting

112
Q

What is the hypothesised causes of eczema?

A
  1. Inside out hypothesis —> immune system pathology results in destruction of the dermis
    1. Outside in hypothesis —> disruption of the dermal barrier causes immune hypersensitivity
113
Q

How is eczema diagnosed?

A
  1. There are no tests

2. Inspection, history and attention age is the most important factors used

114
Q

What is psoriasis?

A

Chronic inflammatory skin disorder that occurs as a result of an autoimmune disorder.

115
Q

What immune response drives Psoriasis and Malar Rash?

A

TH1 overactivity

116
Q

What are some types of psoriasis?

A
  1. Plaque —> most common —> erythematous areas of flaking skin lesions
    1. Inverse —> smooth areas of erythema normally breast, axilla and groin regions
    2. Guttate —> appears soon after respiratory tract infection caused by beta haemolytic streptococcus —> occurs mainly of trunk as small erythematous papules
    3. Erythrodermic —> severe, scaly erythematous lesions over most of body —> often present with systemic effects of fever and dehydration.
    4. Pustular —> uncommon but presents as non infectious pustules.
117
Q

What is the pathophysiology of psoriasis?

A

Autoimmune disorder —> T-cell hyperactivity —> increased pro inflammatory mediators —> cutaneous manifestations —> hyperkeratosis

118
Q

How is psoriasis diagnosed?

A

No definitive lab tests available —> diagnosis mainly based on inspection and history with tests used to exclude other skin disorders

119
Q

What is Malar rash?

A

A purple or red facial rash that appears in a butterfly pattern over nose and cheeks

120
Q

What are some causes of Malar rash?

A

Rosacea (adult acne)
Lupus Seborrheic dermatitis
Photosensitivity (sunlight)
Erysipelas (streptococcus bacteria)
Cellulitis Lyme disease (Accompanied by joint pain, flu like symptoms etc)
Bloom syndrome (Inherited chromosomal disorder pigmentation and intellectual disability)
Homocystinuria (genetic disorder disability leads to vision problems and intellectual disability

121
Q

What can malar rash be triggered by?

A

Stress
Spicy food
Hot drinks
Alcohol

122
Q

What is an Urticarial rash?

A

Urticarial rash is defined as an intensely pruritic rash of erythematous, irregular raised welts (wheals) which usually subsides within 24 hours of ceasing of the drug.

123
Q

What immune response drives Urticarial rash?

A
  • Type 1 hypersensitivity –> Mast cell mediated

- Can also be non-immunologically mediated

124
Q

What can cause Urticarial rash?

A 
Food
Medications
Infections 
Physical stimuli --> sun, exercise
Insect stings
ETC
125
Q

What drugs most commonly cause urticarial rash?

A

Antibiotics
NSAIDS
Anticonvulsants

126
Q

What is Scarlett fever caused by?

A

Group A streptococcus infections

127
Q

What are some symptoms of Scarlett fever?

A 
Sore throat
Fever
Headache
Lymphadenopathy
Erythema due to erythrogenic toxin
128
Q

What are squamous cell carcinomas?

A

Malignancy stemming from the keratinocyte cell lineage

129
Q

Where do SCCs occur?

A

Any cutaneous surface

130
Q

What are Basal cell carcinomas?

A

Common skin cancer arising from the basal layer of the epidermis and its appendages

131
Q

Where do BCCs commonly occur?

A

Face (85%) –> most sun exposure

132
Q

What are the three clinical growth patterns of Basal cell carcinomas (BBC)

A
  1. Superficial BBC —> Trunk and limbs, presents as a erythematous, defined lesion and may be macular or scaly.
  2. Nodular BBC —> Translucent papule or nodule, may have telangiectasia (small dilated vessels close to the skin), as the lesion grows the borders become rolled, can ulcerate and bleed
  3. Infiltrative/Morphoeic BBC —> Present as a sclerotic lesion that is pale and scar aggressive and invade deeper than other BCCs.
133
Q

What are the ABCDEs of malignant melanomas?

A

A —> Asymmetrical
B —> Border (irregular)
C —> Colour (change + non uniform colour)
D —> Diameter above 6mm and continues to grow
E —> evolving surface

134
Q

What are the main drug categories used in allergic responses?

A

Antihistamines
Adrenaline
NSAIDs
Corticosteroids

135
Q

What is the histamine precursor?

A

Histidine

136
Q

What catalyses the reaction from Histadine to Histamine?

A

Histadine Decarboxylase

137
Q

What is the material that histamine is made from?

A

Like other neurotransmitters it is made from amino acids (histadine)

138
Q

Where is histamine found and what is its main role?

A
  1. Main role = inflammation and regulation of the immune response
    1. Large amounts found in mast cells, platelets and basophils
    2. Also found in blood vessels to contact smooth muscle, cardiac mast cells, enterochromaffin like cells of the stomach
139
Q

How to mast cells response to allergen?

A

Release histamine —> which promotes further histamine release as histamine is self-promoting

140
Q

What does mast cell histamine release do for allergy?

A

Promotes recruitment of immune cells

Activate sensory nerve terminals associated with itch, pain and sneezing

141
Q

What is the symptoms of mast cell histamine release?

A
  1. Itch, pain, sneezing
  2. Widespread vasodilation —> swelling of tissue around airways —> hypotension —>shock(haemodynamic) —> death
  3. Marked bronchoconstriction —> laboured breathing, possible asphyxiation huge variation in intensity depending on the person
142
Q

How do antihistamines work?

A
  1. Histamine receptor “blockers”

2. Originally thought to be antagonists has now been discovered that they are actually inverse agonists

143
Q

How does agonists and inverse agonists differ?

A

Agonists bind to a receptor –> cause a conformation change –> increase receptor activity
Inverse agonists bind to a receptor –> cause a conformation change –> decrease receptor activity

144
Q

What does an inverse agonist do eg histamine?

A

Reverse activated state of the receptor and reduces response.
But like a classical agonists does cause a shape change in the receptor.

145
Q

When would an inverse agonist have its greatest effect?

A

When the receptor is constitutive active (receptor is always on without a ligand)

146
Q

What is the effect of a concentration response curve of an inverse agonist and agonists in response to an antagonist?

A

The presence of an antagonist will push the curve to the right.
Antagonists have an effect on both agonists and inverse agonists

147
Q

What is the effect of an antagonists concentration response curve in the presence of agonists and inverse agonists?

A

The response can be “rescued” so will gain some receptor activity

148
Q

How does antihistamines have so many effects?

A

Their mechanism results in different effects in different cell types

149
Q

What is the core mechanism of action for antihistamines in allergy?

A
  1. Reduce H1 histamine receptor activation
  2. Reduce Phospholipase C activation
  3. Reduce IP3 and DAG levels in the cell
  4. Reduce IP3 mediated release of SR calcium stores
  5. Less intracellular Ca2+ (this then drives different responses depending on target cell)
150
Q

Effect of antihistamine mediated Ca2+ reduction in mast cells?

A
  1. Reduces Ca2+ mediated vehicle release (reduces released histamine)
  2. Reduce recruitment of immune cells (mechanism unclear)
151
Q

Effects of antihistamines Ca2+ reduction in neurons responsible for itch pain and sneeze?

A
  1. Reduced kinase activation
  2. Reduced ion channels and receptor activation related to excitability
  3. Reduces itch, sneeze, pain etc.
152
Q

How does antihistamine help with tissue swelling in the airways? (Not really by Ca2+)

A
  1. Reduces vasodilation to help hypotension and fluid accumulation in tissues
  2. Reduces release of NO nitric oxide
  3. Reduces cGMP = increase excitation- contraction coupling
  4. Promotes vasoconstriction
153
Q

How does antihistamines reducing Ca2+ help in bronchospasm?

A
  1. Less Ca2+ = less excitation-contraction coupling
  2. Loss of smooth muscle contraction
  3. Drives bronchodilation (but is not classified as a “true” bronchodilator)
154
Q

What are the two subdivided classes of antihistamines and what is the difference?

A
  1. First generation —> cross BBB to cause sedation/drowsiness
  2. Second generation —> less likely to cross (but sedation can still be an issue with increased concentration or effect
155
Q

What is required for anaphalaxis?

A

Requires a previous exposure to the allergen

156
Q

Why is adrenaline used instead of antihistamine for anaphalaxis?

A

Speed of action faster for adrenaline

157
Q

What are the targets of adrenaline to assist in anaphalaxis?

A

Blood vessels —> A1 receptors for vasoconstriction

Bronchiolar smooth muscle —> B2 receptors driving dilation

158
Q

How does adrenaline drive vasoconstriction with a1 receptors?

A
  1. Activate a1 receptors
  2. Activate Phospholipase C
  3. Increase IP3 and DAG
  4. Promotes IP3 mediated release of SR Ca2+
  5. Increase Ca2+ drives vasoconstriction (increases BP and reduces tissue swelling)
159
Q

Mechanism of action for adrenaline driven bronchodilation?

A
  1. Activate B2 adrenergic receptors on bronchiolar smooth muscle
  2. Activate adenylate cyclase (AdCy)
  3. Increase cAMP levels
  4. Activate protein kinase A
  5. Reduce activation of voltage gates Ca2+ channels
  6. Reduced Ca2+ causes bronchodilation
160
Q

How is anaphylaxis managed/treated?

A

Adrenaline intramuscular injection
High flow oxygen and airway support if needed
If hypotensive –> IV saline
If response is inadequate:
Continue IM adrenaline every 3-5mins
IV adrenaline infusion (not bolus) –> because can drive tachycardia and blood loss to organs

161
Q

How common are streptococcal infection?

A

Cause 20-30% of pharyngitis —> 20% of school age children are carriers

162
Q

How do streptococcal infections normally manifest?

A

Pharyngitis and impetigo

163
Q

What are some immediate complications of streptococcal infections?

A

Symptoms of infection

164
Q

What are some post infection complications of streptococcal infections?

A

ARF, RHD, Toxic shock syndrome

165
Q

What tests are used to identify streptococcal infections?

A
  1. Inspection
  2. Culture
  3. Blood test for antibodies to strep (detects current or past infection)
166
Q

What is C-reactive protein used for in clinical settings?

A

C-reactive protein (CRP) is used to detect inflammation in acute conditions.

167
Q

What are the barriers for prevention of RHD?

A

Needing treatment for any GAS infection which will reduce chance of recurring ARF which then reduces the chance of developing RHD.

168
Q

What is RHD harder to prevent/treat?

A

Poverty
Overcrowding
Access to medical facilities

169
Q

What are disease registers and how do they assist in management of ARF and RHD?

A

They are collections of data on patients/disease/treatment/outcomes. They can be used to identify risk factors and interventions that may be successful.

170
Q

What is atopy vs allergy?

A

Atopy is the genetic predisposition to reacting to allergens. Leading to an exaggerated IgE mediated immune response —> all atopic disorders are type 1 hypersensitivity.

An allergy is any exaggerated immune response to an allergen

171
Q

What is the role of IgE in atopic illness?

A

IgE responds to an allergen and begins an immune response —> in atopy there can be an elevated IgE in the blood as well as general IgE sensitivity.

172
Q

What causes anaphylaxis?

A

Can be immune or non immune causes —> caused by the release of mediators from immunological cells (mast and basophils?)

173
Q

What are the symptoms of anaphylaxis?

A

Skin —> hives, itchiness, swelling
Respiratory —> SOB, wheeze (from bronchial spasm), stridor (upper airway obstruction)
Cardiac —> tachycardia, massive BP drop, (shock)
GIT —> cramps, abdo pain, diarrhoea, vomiting

174
Q

What is the role of antihistamines vis adrenaline in the treatment of anaphylaxis?

A

Adrenaline —> very fast —> best outcomes

Antihistamines—> slower but sometimes used

175
Q

What is the difference between an allergy and an intolerance?

A 
Allergy = immune response to allergen
Intolerance = adverse reaction but does not utilise the immune system
176
Q

What social determinants of health can be linked to disease like RF in ABTIs?

A
  1. Location
    1. Treatment for GAS
    2. Frequency of dr visits
    3. Poverty
    4. Adherence to treatment
    5. Lifestyle factors
    6. Overcrowding
    7. Etc
177
Q

What is the Bradford hill criteria?

A

It is known as the criteria for causation –> useful in establishing epidemiological evidence of a causal relationship between a presumed cause and observed effect relationship

178
Q

What is the 9 Bradford hill criteria?

A
  1. Strength –> effect size (how large the association is)
  2. Consistency –> reproducibility
  3. Specificity –> the more specific an association the more likely a causal relationship
  4. Temporality –> Effect has to occur after the cause/exposure and a delay
  5. Biological gradient –> greater the exposure = a greater incidence of effect
  6. Plausibility –>plausible mechanism between the cause and effect
  7. Coherence –> Epidemiological findings and lab results show a similar pattern
  8. Experiment
  9. Analogy –> similarities between the potential cause and effect and other proven cause and effects
179
Q

What is the concept of natural history of disease?

A

The course a disease takes from its pathological onset until its eventual resolution by full recovery or death

180
Q

What is the concept behind spectrum of disease?

A

The disease process may result in illness that ranges from mild to severe or fatal. This range is called thespectrum of disease.

JMP Y2S1 (24 decks)

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