Answer: Psoriasis vulgaris is a T-lymphocyte-mediated autoimmune skin disorder that involves focal formation of inflamed, raised skin plaques that constantly desquamate scales as a result of excessive epithelial cell growth. There is leucocyte skin infiltration, primarily by T-lymphocytes and neutrophils, hyperplasia of keratinocytes and vascular hyperplasia and ectasia.

Answer: Eczema is an inflammatory condition of the skin associated with epidermal barrier dysfunction. Eczema can affect people across the lifespan and is most commonly diagnosed before the age of 5.

Answer: Atopic eczema is thought to occur as a result of a genetic predisposition and an environmental trigger typical of allergens. The result is a loss of natural moisturisers in epidermis, most notably to the corneocytes whereby the lipid layer is lost, leading to cellular dehydration and subsequent shrinking and cracking of the cell. This change in cellular structure interrupts the protective layer of the epidermis, allowing pathogens access through the gaps and cracks that occur. These pathogens are then detected, triggering the inflammatory response.

Answer: Severe adverse drug reactions are the trigger and the first line of treatment is to cease administration of the offending drug.

Answer: Granulysin.

Answer: Type VII collagen, a component of the anchoring fibrils of the dermal–epidermal junction, is targeted for destruction which causes the epidermis to slough from the dermis.

Answer: Impetigo is a common infection of the superficial layers of the epidermis commonly caused by gram-positive bacteria and is highly contagious. Erythematous plaques with a yellow crust are the most common presentation and the area may be itchy or painful to touch. Impetigo is common in children, with around 10% incidence.

Answer: 

• Bacterial adherence to host cells
• Invasion of tissue with evasion of the person’s host defences
• Distribution of toxins

Answer: Vitiligo is a complex multi-genetic HLA-linked autoimmune disorder whereby there is development of autoreactive T cells and/or inefficient regulatory T-cell function. Additionally, there is development of an anti-melanocyte immune response as part of the condition. Destruction of melanocytes leads to the depigmentation. First-grade relatives have a 6–8% risk of developing vitiligo; this increases to 23% in monozygotic twins.

Answer: 

1. Propionibacterium acnes (P. acnes) proliferation: P. acnes stimulates the release of proinflammatory cytokines that lead to an inflammatory process. However, recent opinion is that the microbiome itself is disturbed, rather than P. acnes being responsible for this cytokine release.
2. Keratinocyte hyperproliferation in the follicle: Disrupted follicular keratinisation is a key component of pore blockage in acne. Hyperproliferation of keratinocytes can occur when there are changes in sebum production.
3. Androgen-mediated increase in sebum production: Sebum production is triggered by androgen activity in the pilosebaceous unit. In acne, it is thought that excess androgens or a hypersensitivity to normal androgen levels may result in the increase in sebum production seen. Additionally, increased activity of 5α-dihydrotestosterone (5α-DHT) in the skin may also cause this increase in sebum production.
4. Inflammation: Inflammation is thought to occur as a result of one of two processes. Either follicular hyperkeratinisation triggers an inflammatory process, or inflammation itself triggers an increased proliferation of keratinocytes.

Answer: The anagen phase

Answer: A wound that occurs in the upper layers of the skin secondary to sustained, externally applied pressure that causes localised ischaemia and an inflammatory response. This wound then enlarges radially and deeper into tissue layers unless the underlying causes are addressed to counteract the course of events.

Answer: Both are musculoskeletal injuries, however they differ in relation to the tissues affected.

• Strains involve damage to tendons (tissue that joins muscle to bone)
• Sprains involve damage to ligaments (tissue that joins bone to bone).

Answer: Osteopenia is common to all metabolic bone diseases, it is not a diagnosis but rather it is used to describe bone density loss that is seen on X-ray. The reduction in bone density is greater than what would be expected for age, gender or race.

The major causes of osteopenia include: osteomalacia, osteoporosis, hyperthyroidism and hyperparathyroidism.

Answer: Osteoporosis can be either primary (postmenopausal osteoporosis) or secondary.

• Primary osteoporosis has unknown aetiology but is thought to occur with ageing and is accelerated at menopause.
• Secondary osteoporosis is due to an underlying condition, e.g. Cushing’s syndrome.

Answer: There are a number of factors that may predispose a person to osteoporosis, these include: ageing, hormonal imbalances/endocrine dysfunction, other medical conditions, insufficient intake or malabsorption of vitamins and minerals, excessive intake of alcohol, caffeine and nicotine, decrease in activity or weight bearing activities and certain drugs.

Answer: Vitamin D

Answer: OA can affect both central and peripheral joints and is commonly found in the knees, hips, spine, shoulder, lower cervical, lumbosacral vertebrae, hands and wrists but may occur in any synovial joint.

Answer: 

• Inflammatory cytokines include: tumor necrosis factor-alpha (TNF-a) and interleukins 1beta (IL-1b) and interleukin-6 (IL-6).
• Enzymes include: metalloproteinase, collagenase, elastase and PGE₂

Answer: 

• Duchenne muscular dystrophy (DMD) is an inherited X-linked recessive trait and is considered the most severe form.
• Becker MD shares the same genetic locus as DMD, however, those with BMD present later in childhood and their progression is usually slower and less severe.
• Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant inherited disorder and is one of the most common muscular dystrophies.

Myotonic muscular dystrophy (MMD) occurs due to mutations in either of two genes causing type 1 (DMPK gene) and type 2 (CNBP gene) MMD.