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Medicine Sem 1 > Case 6 > Flashcards

Case 6 Flashcards

1
Q

What are Type I hypersensitivities? what do they include? what is their prevalence in developed countries? how long does it last? who is affected more, children or adults? and how is it treated?

A
  • Atopy (out of place)
  • Food allergy, asthma, rhinitis, systemic anaphylaxis (serious allergic reaction that is rapid onset and may cause death), eczema
  • Asthma: 5-17%
  • Allergic rhinitis: 10-20%
    (often asthma and hay fever go together)
  • Food allergy: 1-2% adults; 5-8% children
  • Eczema: 1 in 5 children, 1 in 12 adults
  • Systemic anaphylaxis (food allergy, insect stings, medications): 150 fatalities per year in US; >50% in teenagers
  • Sensitisation can be irreversible and life-long
  • Children affected more commonly than adults
  • There is no cure
  • Treatment is for symptoms
  • AVOIDANCE
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2
Q

Describe the steps in a Type I hypersensitivity reaction.

A

Sensitisation:
1. The Fc part of IgE binds to FcER on mast cells/basophils, exposing it variable region – this IgE loading takes 10-15 days
2. This is the sensitisation phase as the mast cells/basophils are ready to work the next time the pollen appears
3. When the antigen reappears, they will come into contact with sensitised (IgE-loaded) mast cells and stimulate it and cause an initial phase reaction and a secondary reaction
Initial phase reaction:
1. Upon stimulation, the mast cells undergo degranulation, secreting preformed produced (primary mediators) – these include histamine and proteaasea
- The proteases will do further tissue damage, causing the release of more inflammation mediators
2. The histamine has the following effects:
- Vasodilation
- Increased vascular permeability leading to partial edema in the area
- Spasmatogenic: histamine receptors are found on the smooth muscle lining of the various tracts – histamine causes them to contract
- Increasing glandular secretions, causing luminal obstruction
- Overall, histamine causes narrowing of the lumen of the tract
Secondary reaction:
1. Upon stimulation, the mast cells secrete cytokines (IL-3, IL-5 and leukotrienes)
2. The cytokines are termed secondary mediators as they are not preformed
3. IL-3 and IL-5 are chemotactic agents for eosinophils
4. Leukotrienes attract neutrophils
5. Eosinophils secrete their granular contents: histaminases (reducing inflammation) and enzymes that destroy leukotrienes (reducing attraction of neutrophils)

Mast cells are very sensitive and can be stimulated by many factors, some of which include:

  1. Cross-linking of loaded IgE by multivalent antigens
  2. Venoms such as that from a bee sting
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3
Q

What is anaphylactic shock? what happens during it?

A

Systemic type I hypersensitivity reaction

  • Circulation allergen (e.g. penicillin) affects mast cells throughout the body
  • Extensive peripheral vasodilation, producing a fall in blood pressure that can lead to a circulatory collapse – this response is anaphylactic shock
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4
Q

What is the treatment for type I hypersensitivities?

A

Antihistamines

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5
Q

What is the acute response in Type I hypersensitivities?

A
  • Mast cell degranulation
  • Airway obstruction
  • Leaky blood vessels
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6
Q

What is the late phase response of type I?

A

Recruitment of eosinophils and Th2 cells from circulation

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7
Q

What is the chronic response of type I?

A
  • Release of cytokines (Th2 cells)

- Eosinophil granule proteins = chronic inflammation -> make airways smaller as they remodel them

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8
Q

What happens in the skin, airways, GI tract, and blood vessels in a Type I hypersensitivity?

A

Skin
- Increased blood flow, increased permeability
- Increased fluid, redness, swelling, rashes
Airways
- Decreased diameter, increased mucus
- Congestion of airways, swelling/mucus secretion
GI tract
- Increased fluid secretion, increased peristalsis
- Expulsion of GI tract contents
Blood vessels
- Increased blood flow, increased permeability
- Increased tissue fluid, lymph flow to lymph nodes, cells/proteins in tissues

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9
Q

What is activated in the skin, inhalation, gut, high dose intravenous, and what does this cause?

A

Skin -> mast cell activation -> local histamine wheal and flare
Inhalation -> mast cell activation -> allergic rhinitis asthma
Gut -> mast cell activation -> vomiting, diarrhoea
High dose intravenous -> mast cell, basophil (positive feed-back route – rapid inflammatory response) activation -> systemic histamine release – anaphylaxis (epi-pen needed)
Gut -> (if a lot of mass cell degranulation of high IgE antibody) -> mast cell, basophil activation -> blood stream (as blood vessels are leaky) -> anaphylaxis

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10
Q

How is a Type I hypersensitivity diagnosed?

A

Detection of IgE
- Specific serum IgE ex vivo
- Skin prick test/prick to prick tests (into fruit then into skin)
Provocation challenge – costly
Food allergy: (double-blind placebo controlled food challenge)
Rhinitis: nasal challenge
Asthma: bronchial provocation test

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11
Q

What is the treatment?

A

Pharmacotherapy for symptoms:

  • Anti-histamines
  • Mast cell stabilising compounds
  • Topical and systemic corticosteroids
  • Generally, provide moderate or partial relief; severe cases often refractory

For systemic anaphylaxis = adrenalin (EpiPen)

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12
Q

What is a Type IV hypersensitivity? what is the process? what are the two types? how does it begin? and what are examples?

A
  • Delayed hypersensitivity
  • Cell-mediated reaction (only immune cells involved and not antibodies) in which the signs appear about 12 to 72 hours after exposure
  • Allergens have haptens which are too small to initiate an immune response
  • Haptens bind to host haptenated proteins
  • These produce new antigens which are taken up by Langerhans and presented
  • Only activation of Th1 CD4 cells and macrophages
  • These are two types:
    1. Delayed type hypersensitivity reaction
    2. T-cell mediated cytotoxicity
  • It begins when APCs in the lymph nodes display allergens to helper cells
  • CD4 cells secrete interferon-Y which activates macrophages
  • CD4 cells secrete IL-2 which activates T-cytotoxic cells
  • Examples: type 1 diabetes mellitus, Crohn’s disease and mulitple sclerosis
  • Common occupational issue - contact allergens
  • Mediated by Th1 cells/Tc cells
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13
Q

What is the test for TB?

A

The Mantoux test

  • involves intradermally injecting the TB antigen
  • waiting for CD4 and CD8 cells to react to virus
  • then waiting for a response in the skin
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14
Q

What is the mechanism of a Type IV reaction?

A
  • Th1 cells misrecognise the chemicals as viruses and intracellular bacteria
  • Exposure through skin of allergen
  • Allergen picked up dendritic cells and taken to the lymph node where you get clonal expansion of allergen-specific T lymphocytes = primed
  • The next time you see the allergen, the T cells are in the skin, they see the allergen, and produce cytokines which recruit macrophages
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15
Q

What is the elicitation reaction for type IV?

A
  • Antigen is processed by tissue APC (antigen-presenting cells) – dendritic cells and macrophages
  • Stimulates Th1/Tc1 cells
  • Chemokines released – recruit macrophages to site of antigen deposition
  • Cytokines released – IFN-gamma activated macrophages, IL3/GMCSF stimulate monocyte production
  • Cytotoxins released – TNFalpha/beta cause local tissue destruction and increase adhesion molecule expression
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16
Q

How do you diagnose these allergies?

A

Patch testing

- wait a few days to see what they reacted to

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17
Q

What is treatment for these allergies?

A
  • Identification of allergen and avoidance
  • Mid to high potency topical corticosteroids
  • Extensive (>20%): systemic steroids
  • No cure
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18
Q

What is the antigen form in Type I and Type IV hypersensitivities?

A

Type I = soluble antigen

Type IV = soluble or cell-bound antigen

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19
Q

What is a summary of the mechanisms of activation for both hypersensitivities?

A

Type I = allergen-specific IgE antibodies bind to mast cells via their Fc receptor - when the specific allergen binds to the IgE, cross-linking of IgE induces degranulation of mast cells
(degranulation is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells)

Type IV = Th1 cells secrete cytokines, which activate macrophages and cytotoxic T cells

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20
Q

What is Staphylococcus aureus? what’s its shape? where’s it found? what does ti commonly cause? how does it work? in which patients is it particularly prevalent in? what is the treatment? what is the mechanism for how it gets in?

A
  • Bacterium
  • Cocci shaped (round)
  • Gram-positive bacteria
  • Found in the human respiratory tract and on the skin
  • It isn’t always pathogenic, but it is a common cause for skin infections, by breaching the barrier (e.g. in dry skin)
  • Disease-associated strains of S. aureus often promote infections by producing potent proteins toxins, and expressing cell-surface proteins that bind and inactivate antibodies
  • The emergence of antibiotic-resistant forms of pathogenic S. aureus (e.g. MRSA) is a worldwide problem in clinical medicine
  • S. aureus is extremely prevalent in atopic dermatitis patients – it’s mostly found in fertile, active places, including the armpits, hair, and scalp
  • Treatment: penicillin – however, penicillin resistance is extremely common, and first-line therapy is most commonly a penicillinase-resistant B-lactam antibiotic (for example, oxacillin or flucloxacillin)
  • Mechanism: patient scratches the skin due to the itching which breaks the epidermis of the skin – S. aureus is found on the skin – upon scratching, the bacteria enter the skin, causing infection
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21
Q

What are the functions of the skin?

A
  1. Protection: against UV light, keratinisation and physical barrier
  2. Immunological barrier: inflammation, infection and sebaceous glands
  3. Sensation: contains a range of different receptors for touch, pressure, pain and temperature
  4. Thermoregulation: hair, subcutaneous adipose tissue (insulation), sweat glands, vasodilation and vasoconstriction
  5. Metabolic functions: the most important metabolic function is the synthesis of vitamin D3 by the action of UV light. The adipose tissue in the subcutis is a major store of energy in the form of triglycerides
  6. Water conservation: water-resistant, not waterproof
    - Many bacteria live on the human skin (e.g. Staphylococcus aureus)
    - The skin is not a good site for micro-organisms: dry, slightly acidic and hyperosmotic (salt from sweat glands)
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22
Q

Describe the epidermis. What is it made up of? how do the cells get oxygen and nutrients? what is it dominated by? how long does maturation take?

A
  • Keratinised stratified squamous epithelium
  • Avascular – the epidermal cells rely on the diffusion of nutrients and oxygen from the capillaries within the dermis – as a result, the epidermal cells with the highest metabolic demand are found close to the basal lamina, where the diffusion distance is short – the superficial cells are either inert or dead
  • Dominated by keratinocytes – the body’s most abundant epithelial cells
  • Maturation takes about 28-30 days
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23
Q

How many layers does the epidermis have? and what are the layers?

A
  • Thin skin, which covers most of the body surface contains four layers of keratinocytes
  • Thick skin, which occurs on the palms of the hands and the soles of the feet, contains a fifth layer, the stratum lucidum – the has a much thicker superficial layer (stratum corneum)

Layers:

  • stratum basale
  • stratum spinosum
  • stratum granulosum
  • stratum lucidum
  • stratum corneum
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24
Q

What does the stratum basale consist of? and what does its components do?

A
  1. Keratinocytes: germ cells of the epidermis – their divisions replace the more superficial keratinocytes that are lost or shed at the epithelial surface – as these move to the more superficial layers, the cells become flattened
  2. Melanocytes: pigment-producing cells, responsible for skin colour – melanosomes (vesicles responsible for synthesis, storage and transport of melanin) provide protection from UV radiation and convert a precursor into cholecalciferol (inactive vitamin D3). Cholecalciferol is hydroxylated (+ -OH) to calcifediol/calcidiol (25hydroxyvitamin D3) in the liver. Calcifediol is hydroxylated into calcitriol (1,25dihydroxyvitamin D3 - active vitamin D3) in the kidney.
  3. Merkel cells: light touch receptors.
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25
Q

What attach the cells of the stratum basale to the basal lamina (basement membrane)?

A

Hemidesmosomes

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26
Q

What does the stratum spinosum consist of?

A
  1. 8-10 layers of keratinocytes (divisions of the germ cell keratinocytes from the stratum basale)
  2. Spiny layer: cells are held together by spiny projections called desmosomes
  3. The keratinocytes continue to divide and push superficial into the stratum granulosum
  4. Keratinocytes start producing keratin and keratohyalin
  5. Keratin is the basic structural component of hair and nails in humans
  6. Contains Langerhans Cells (dendritic cells (phagocytes))
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27
Q

What does the stratum granulosum consist of?

A
  1. 3-5 layers of keratinocytes derived from the stratum spinosum
  2. Grainy layer: contain granules of keratohyalin
  3. Keratohyalin is a protein which promotes dehydration of the cell and crosslinking of keratin fibres
  4. Upon reaching the stratum granulosum, the keratinocytes stop dividing
  5. The layer forms epidermal ridges, which extend into the dermis and are adjacent to dermal projections called dermal papillae that project into the epidermis
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28
Q

What does the statum lucidum?

A
  1. A clear (glassy) layer in thick skin, which covers the stratum granulosum
  2. Fattened, densely packed cells filled with keratin
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29
Q

What does the stratum corneum consist of? what is a property of this layer? and how are blisters formed?

A
  1. Most superficial layer
  2. 15-30 layers of keratinized cells
  3. Keratinisation, or cornification, is the formation of protective, superficial layers of cells filled with keratin
  4. Dead cells in stratum coreum remain tightly interconnected by desmosomes
  5. This layer is usually dry, so it is unsuitable for the growth of many microorganisms. Maintenance of this barrier involves coating the surface with lipid secretions from sebaceous glands
  6. This layer is water resistant, but not waterproof. Water from the interstitial fluids slowly penetrates the surface, to be evaporated: 1. Insensible perspiration: perspiration where we are unable to see or feel the water loss. We lose roughly 500ml of water this way each day. Damage to the epidermis increases the rate of insensible perspiration (dehydration/xerosis (dry skin)). 2. Sensible perspiration: perspiration where we are aware of it, as a result of active sweat glands
  7. If damage breaks connections between superficial and deep layers of the epidermis (or between epidermis and dermis), fluid will accumulate in the pockets (blisters).
30
Q

What causes epidermal pigmentation? what causes people to have darker skin? what is the importance of the melanin in keratinocytes?

A
  • Melanocytes synthesise melanin from the amino acid tyrosine and package it in intercellular vesicles called melanosomes
  • These vesicles travel within the processes of the melanocytes and are transferred to keratinocytes
  • In darker people the melanosomes are larger
  • The melanin in keratinocytes protects the dermis and the epidermis from the harmful effects of UV radiation
31
Q

What does the dermis consist of?

A

The dermis composes of connective tissue and has two major components: a superficial papillary layer and a deeper reticular layer

32
Q

What does the papillary layer of the dermis consist of? and what condition is this layer involved in?

A
  • Layer derives its name from the dermal papillae that project between the epidermal ridges
  • Consists of fibrous connective tissue: fine and loosely arrange collagen fibres
  • Consists of blood vessels (papillary plexus)
  • Dermatitis is an inflammation of the skin that primarily involves the papillary layer
33
Q

What does the reticular layer consist of?

A
  • Consists of irregular connective tissue which provide strength and elasticity:
    1. Collagen: very strong and resist stretching, but are easily bent or twisted
    2. Elastic fibre: permit stretching and then recoil to their original length
    3. Water content (skin turgor) also helps maintain flexibility – one sign of dehydration is loss of skin turgor
  • Consists of extrafibrillar matrix
  • Consists of:
    1. Mechanoreceptors:
  • Meissener’s corpuscle: light touch receptors
  • Pacinian corpuscle: pressure and vibration receptors
  • Free nerve endings: pain and temperature receptors
    2. Hair follicles
    3. Arrector Pili Muscle: contraction causes the hair to become erect and sebaceous glands to secrete sebum
    4. Sweat glands: apocrine and merocrine (eccrine)
    5. Sebaceous glands
    6. Blood vessels: cutaneous plexus – trauma to the skin often results in contusion (bruise) as a result of the rupture of dermal blood vessels (both plexuses)
    7. Lymphatic vessels
  • Consists of:
    1. Macrophages
    2. Mast cells
34
Q

What are the accessory structures? where do they originate from? and where are they located?

A
  • Hair, hair follicles, sebaceous glands, sweat glands and nails
  • During embryological development, these structures originate from the epidermis and are so called epidermis derivatives
  • Although located in the dermis, they project through the epidermis to the surface
35
Q

What do sebaceous glands? how do they do this? and what does sebum do?

A
  • Secrete an oily lipid secretion (sebum) into hair follicles
  • The arrector pili muscles contract, squeezing the sebaceous gland and secreting sebum
  • Sebum:
    1. Inhibits the growth of bacteria
    2. Lubricates skin
36
Q

What are the two types of sweat glands? where are they found? what do they secrete? which ones start secreting at puberty? size? and how widely spread?

A
  • Two types of sweat glands:
    1. Apocrine sweat glands:
  • Found in armpits (axillae), around nipples and in the pubic region
  • Secrete products (via membrane budding) into hair follicles
  • Start secreting at puberty
  • Sweat is a nutrient source for bacteria, which intensify its odour
    2. Merocrine (eccrine) sweat glands:
  • Secrete products (via exocytosis) directly onto the surface of the skin
  • More widely spread than apocrine sweat glands
  • Smaller than apocrine glands
  • Sweat produced is called sensible perspiration
37
Q

What are the functions of sweat glands?

A
  1. Cooling the surface of the skin to reduce body temperature
  2. Excreting water and electrolytes
  3. Providing protection from environmental hazards
38
Q

Why is the hypodermis (subcutaneous layer) important? what does it consist of? and what do these components do?

A
  • It’s important in stabilising the position of the skin in relation to underlying tissue, such as skeletal muscles or other organs, while permitting independent movement
  • Consists of:
    1. Adipose tissue
    2. Fibrous connective tissue – making it quite elastic
    3. Blood vessels: cutaneous plexus
  • Subcutaneous injections: by means of a hypodermic needle
  • Subcutaneous fat provides insulation, serves as a substantial energy reserve and as a shock absorber
39
Q

What are the different types of junctions?

A
  • Tight junctions: the area where two cells whose membranes join together to from a virtually impermeable barrier to fluid
  • Gap junctions: specialised intercellular connection between cells – it directly connects the cytoplasm of two cells, which allows various molecules and ions to pass freely between the cells
40
Q

What are the functions of B lymphocytes (antibodies)?

A
  • Toxin neutralisation
  • Complement lysis of bacteria
  • Facilitates internalisation for intracellular killing by neutrophils and macrophages
  • Parasite expulsion (inflammatory reactions)
  • Passive immunity by transplacental transfer
41
Q

Describe the kinetics of antibody response to infection.

A

First infection:

  • Initial immune response
  • Lag phase to respond
  • Low affinity (low affinity antibodies are produced early immune responses and are followed by high-affinity antibodies later and in memory B-cell responses)
  • IgM tends to be the antibody that’s produced

Second infection:
- Secondary response
- Higher affinity and other isotypes of immunoglobulin
- IgG is the most common switch
- If in the mucosa, it goes to IgA
(the Ig isotype (class) is encoded by the constant region segments of the Ig gene which form the Fc portion of an antibody – the expression of a specific isotype determines the function of an antibody via the specific binding to Fc receptor molecules on different immune effector cells – isotype expression reflects the maturation stage of a B cell – naïve B cells express IgM and IgD isotypes with unmutated variable genes – expression of other antibody isotypes occurs via a process of class-switch recombination (CSR) after antigen exposure – which switch happens depends on the site of the infection and different stimuli that are coming from that infection)

No apparent symptoms:

  • Immunological memory
  • Next time you get an infection you get a very high affinity response from the antibodies with either IgG, IgA, IgE – depending on the location and the nature of the response
42
Q

Describe how vaccinations work.

A
  • Inject attenuated pathogen – primary response
  • Booster injection – secondary response
  • Subsequent infections: no disease – immunological memory
43
Q

What are the different functions of T lymphocytes?

A
  • Kill virus-infected cells – CD8 cells (difference between these and the NK cells, is that these kills virally-infected cells specifically) – perforin granzymes -> kill cells via apoptosis
  • Resistance against intracellular pathogens
  • Activate macrophages
  • Help antibody responses
  • Immunoregulatory function
44
Q

What is the human leukocyte antigen (HLA) system?

A
  • HLA system is a gene complex encoding the MHC proteins in humans – these cell-surface proteins are responsible for the regulation of the immune system in humans
  • Polymorphic alleles
  • Polygenic, polymorphic (HUGE degree of variation in genes) and codominant
  • Class I = all nucleated cells (host)
  • Class II = B cells, antigen-presenting cells
45
Q

How do intracellular antigens work?

A
  • Endogenous pathway
  • MHC class I molecule operates via the endogenous pathway of antigen processing by the host cells to present it to CD8 T cells
  • The cytoplasmic protein (from the pathogen) is processed and then packaged with MHC class I molecules
  • Proteins are inside the cell because it’s from a virus and so the CD8 T cell responds
46
Q

How do extracellular antigens work?

A
  • Exogenous pathway
  • CD4 T cell responds to MHC Class II
  • Proteins that are outside the cell are taken up by the cell
  • All antigen-presenting cells have different methods of taking up protein – they sample the external environment and take up the proteins
  • Once they’re inside the cell they process the peptides and they’re packaged with MHC class II
  • It’s the MHC class II – peptide complex that the Th cell responds to
47
Q

What are T cell receptors and B cell receptors like?

A 
T cell receptor: (always responds to cell-associated proteins) 
-	Antigen-binding site 
-	Variable regions 
-	Constant regions 
-	Transmembrane region – always a membrane receptor 
-	Alpha chain and beta chain 
B cell receptor: 
= immunoglobulin 
-	Antigen binding site 
-	Transmembrane region 
-	Bivalent receptor 
-	Soluble form of the immunoglobulin receptor = antibody
48
Q

How is the diversity of the receptors created?

A

Germline configuration – variable regions (made up by many gene segments), D (diversity = extra variable) regions, J regions, Constant regions
D to J recombination – genes selected randomly from both regions, and then the intervening bit of DNA is just clipped out
V to DJ recombination – one of the variable genes randomly being selected and then the intervening bit of DNA between that gene and the DJ region is cut out – this consequent VDJ region will make up the variable region of either your B cell or T cell receptor
- B and T cell receptor chains are the product of several genes
- Each receptor chain:
- 2-3 different V gene segments (V, D, J)
- 1 C gene segment
- Random selection of V (variable), D (diverse) and J (joining – of the constant region to the variable region) segments from large gene pool generates >10^7 different antigen specificities AND can generate self-reactive antigen receptors
- The variable region of the heavy chain is made up 3 segments – V, D and - The light chain is smaller and is made up of just V and J segments – that’s why any chain will have 2-3 different segments

49
Q

What is the negative selection of autoreactive B cells?

A

(The many combinations of antigen mean that some might react to self)

  • Occurs in bone marrow (this is what is meant by education)
  • Receptor gene rearrangement generates novel B cell specificities
  • Some may bind self-antigens
  • Encounter with self-antigen causes apoptosis
  • 90% of B cells are destroyed in the bone marrow
50
Q

What is the selection of T cells in the thymus?

A

(more important because they have so many different function)

  • Immature T cells undergo 2 rounds of selection in thymus
  • Positive selection for MHC I and II recognition
  • Negative selection to remove self-reactive T cells
  • About 2% of T cells survive the whole process

Positive selection

  • They have to be able to recognise MHC – either class II if they’re a CD4 cell or class I if they’re a CD8 cell – because they only see their antigen in the context of MHC
  • The ones who don’t react with the antigen undergo apoptosis – No MHC recognition

Negative selection

  • Self-peptide response -> apoptosis
  • No self-peptide response -> exit thymus
  • The thymus express antigens from tissues all around the body
51
Q

How are reactive T cells regulated?

A
  • Mechanism = central tolerance
  • A self-reactive T cell may escape deletion in the thymus
  • In periphery, such self-reactive T cells can be activated
  • But there are number of control mechanisms to prevent activation
    -one is ignorance – it may never meet its antigen
    -anergy – if it meets its antigen the T cell won’t be activated in the same way as it will be lacking signal 2 and 3 – the T cell will be encouraged to undergo anergy where it will forget the antigen
    = peripheral tolerance
52
Q

What is a subpopulation of T helper cells? and what do they do?

A

Treg – T regulatory cells

  • Control of immune responses
  • Preventing allergy autoimmunity
  • They produce cytokine IL-10 and TGFBeta (transforming growth factor) = dampen down immune responses
53
Q

Explain peripheral tolerance. Where are most of the Treg cells?

A
  • T cell specific for self-antigen becomes a Treg
  • Cytokines (IL-10 and TGF) produced by Treg inhibit other self-reactive T cells
  • 1-10% of thymic and peripheral CD4 T cells become Treg cells
  • Most of these treg cells are specific to self-antigens
  • Most of Treg cells in gut – constantly seeing food that you’d don’t want to respond to immunologically but just want to digest
54
Q

What does innate immunity consist of?

A
  • Physical barriers
  • Antimicrobial factors e.g. chemokines & cytokines
  • Phagocytes and natural killer cells
  • Inflammation/fever
55
Q

How does the skin act as a physical barrier?

A
  • Antimicrobials e.g. lactoferrin
  • Low PH
  • Shedding
  • Commensal bacteria – crowding out bad bacteria
56
Q

What are the cellular vectors in the innate immune system? and what are they important for?

A

Phagocytes: neutrophils, monocytes/macrophages – respond to PAMPS (such as polysaccharide in gram negative bacteria & peptide and glycan in gram positive bacteria) & DAMPS (ATP, uric acid, heat shock protein)
Anti-viral killer cells: natural killer cells (by apoptosis)
Antigen-presenting cells: dendritic cells

Following cellular vectors, more important in allergies:
Mast cells/basophils (basophils either die(quickly)or become mast cells in the tissue (survive for long time)) -> contain biogenic amines, lipid mediators, cytokines, enzymes -> vascular leak, bronchoconstriction, intestinal hypermotility, inflammation
- (more mast cells in the body than basophils)
- Protect against large multicellular organisms because a macrophage can’t engulf a multicellular organism -> flushing out the organism
Eosinophils -> contain cationic granule proteins, enzymes -> killing of parasites
- Slightly more common than basophils
- Increase in eosinophils if infection by a multicellular organism

57
Q

What triggers mast cell degranulation?

A
  • Mast cell detects danger and then releases its granules

- Triggered by certain viruses and parasites

58
Q

What are the effects when mast cells undergo degranulation?

A

Skin
- Increased blood flow
Increased permeability (e.g. due to release of histamine)
- Vasodilation,
Endothelial cell activation and cellular recruitment

Airways
- Decreased diameter (as muscles in airways bronchoconstrict)
Increased mucus
- Coughing (expulsion of parasite),
Immobilisation of pathogen by mucus and cyroprotection

Gastrointestinal tract
- Increased fluid secretion 
Increased peristalsis 
- Expulsion of GIT contents (parasites)
Immobilisation of pathogen by mucus and cryoprotection

Blood vessels
- Increased blood flow
Increased permeability
- Increase tissue fluid, lymph flow to lymph nodes, cells/proteins in tissues – activates immune system

59
Q

What are the functions of eosinophils?

A
  • Tissue remodelling (generate epithelial and muscle cells and generally start the process of remodelling) (and clear up debris)
  • Direct toxicity – kill parasites
60
Q

What is used for the management of eczema?

A

Increasing effectiveness, increasing side effects:

  • Topicals (putting a new layer on)
  • bath additives, emollients (creams, ointments)
  • Topicals (protects the barrier, suppresses the inflammation)
  • steroids (topical safer than oral), immunomodulators
  • Phototherapy (light treatment) – light suppresses your immune system
  • UVB, TLO1 (type of UVB), PUVA
  • Systemics
  • systemic steroids – supress the immune system
61
Q

What are topical corticosteroids? what are the forms? what are the potencies? what conditions are they used for?

A
  • Medications applied directly to the skin to reduce inflammation and irritation
    Forms
  • Creams, lotions, gels, mousses, ointments
    Potencies
  • Mild, moderate, potent, and very potent
  • Mild corticosteroids, such as hydrocortisone, can often be bought over the counter, while stronger types are only available on prescription
    Conditions
  • Eczema, seborrheic dermatitis, psoriasis, nappy rash
62
Q

What are emollients? how do they work? what are they often used to manage?

A
  • Moisturising treatments applied directly to the skin to soothe and hydrate it
  • They cover the skin with a protective film to trap in moisture
  • Emollients are often used to help manage dry, itchy or scaly skin conditions such as eczema, psoriasis and ichthyosis
  • They help prevent patches of inflammation and flare-ups of these conditions
63
Q

What is a case report?

A
  • The simplest type of clinical study, in which the medical history of a single patient is described anecdotally (retrospective)
  • Advantages: lots of information can be conveyed that would be lost in a clinical trial, easy to understand, written up in short period of time
64
Q

What is a case series?

A
  • The history of several patients with a similar problem or outcome of interest (retrospective)
  • Advantages: illustrate an aspect of a condition, treatment or adverse reaction, easy to understand, written up in short period of time
65
Q

What is a ecological study?

A
  • Use population data, as opposed to individual records (retrospective)
  • Advantages: conducted on very large-scales using data that are already available, done fairly quickly and inexpensively
66
Q

What is a cross-sectional survey?

A
  • Data are collected from a representative sample of individuals at a specific time, in this way, characteristics of a population are described at a particular point in time (single time, may be retrospective)
  • Advantages: relatively cheap and simple to perform, ethically safe
67
Q

What is a case-control study?

A
  • People with particular outcomes are identified and matched with ‘controls’ – people randomly selected from the same population who do not have the condition of interest – histories of the two groups are then compared (retrospective)
  • Advantages: control group included gives reliable baseline data to compare with, option for studying rare conditions, quick and cheap
68
Q

What is a cohort study?

A
  • Groups of people are selected on the basis of differences in their exposure to a particular agent and followed up over time to see how many people in group develop a particular disease or other outcome (prospective)
  • Advantages: control group included, used when RCTs would be unethical, cheaper and simpler than RCTs, can sometimes be very large, can establish the timing and sequence of events, ethically safe
69
Q

What is a crossover trial?

A
  • Used to compare responses of individual patients to two different treatments for the same condition (prospective)
  • Advantages: because patients act as their own controls, this has the effect of reducing the number of subjects that are required to obtain valid results
70
Q

What is a randomised controlled trial?

A
  • Each participant is randomly assigned to one group or another, the investigator controls the exposure of the factor of interest (prospective)
  • Advantages: control group included, rigorous evaluation of a single variable in a precisely defined patient group, randomisation reduces risk of bias, allow for meta-analysis
71
Q

What is a systematic review?

A
  • High-level overview of primary research on a particular research question that tries to identify………………
  • Advantages: large amounts of information concerning a specific……………

Medicine Sem 1 (8 decks)

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