Week 2 Flashcards
What are the two types of fascia and how do they differ?
Superficial fascia, made up of loose connective tissue and fat
Deep fascia - a tough sheet, dividing regions into compartments
Describe the arterial supply of the upper limb, proximal to distal
Subclavian artery -> axillary artery -> brachial artery -> SPLIT into radial artery and ulnar artery, which give off the deep and superficial palmar arteries respectively (although both these arteries contribute to each palmar arch)
Describe the venous blood supply of the upper limb, distally to proximally
Palmar venous arches drain into the Radial and Ulnar veins, which both drain into the Brachial vein
Dorsal venous network drains into the cephalic and basilic veins. These two are linked in the antecubital fossa by the Median cubital vein.
The Cephalic vein drains into the Axillary vein, and the Basilic vein joins with the Brachial vein to form the Axillary vein.
The Axillary vein then goes on to drain into the Subclavian vein
How do venous ulcers occur?
Where is the most common site?
Immobility/venous valve failure of any cause leads to chronic venous insufficiency, which as well as resulting in deep venous stasis also results in superficial microcirculatory deficiencies = ulcers form
Most common site of venous ulceraction is the “gaiter area” - medial aspect of the distal leg
What are some of the chemical mediators of itch in the skin?
Histamine
PGE2
Acetylcholine
Serotonin
Kallikrein
IL-2
What are the four categories of causes of itch?
Pruritoceptive - something in the skin triggers the itch, associated with inflammation or dryness
Neuropathic - damage of any sort to central or peripheral nerves
Neurogenic - no evident damage in the CNS, but itch is caused by effects on CNS receptors
Psychogenic - psychological cause with no damage to the CNS e.g. itch is a delusion of infestation
Systemic diseases associated with itch mostly are neurogenic causes of pruritus. Give some examples
Haematological
Paraneoplastic
Liver and bile duct
Psychogenic disease
Kidney disease
Thyroid disease
What are some of the treatments used in the management of itch?
Sedative anti-histamines
Emollients
Antidepressants
Phototherapy
Opiate antagonists e.g. ondansetron
(if neuropathic, anti-epileptics)
Where are melanocytes found? What is their function?
At the DE junction, in the basal layer
Melanocytes synthesise melanin, and transfer the pigment to keratinocytes via dendritic processes
What type of collagen makes up the dermis?
Matrix of Type I and Type 111 collagen fibres
What do the following terms mean:
Parakeratosis
Hyperkeratosis
Acanthosis
Papillomatosis
Spongiosis?
Parakeratosis - peristence of nuclei in the keratin layer
Hyperkeratosis - increased thickness of keratin layer
Acanthosis - increased thickness of whole epithelium
Papillomatosis - irregular epithelial thickening
Spongiosis - oedema fluid between squames appears to increase prominence of intercellular prickles
Give a brief definition of Psoriasis
Common chronic inflammatory dermatosis
Epidermal hyperplasia, meaning increased epithelial turnover
Pathogenesis remains elusive
Causes red, flaky, crusty patches with scale
Found commonly on extensor surfaces (knees, elbows, scalp, lower back) but can appear anywhere on the body
Lichenoid disorders are characterised by damage to the basal layer of the epidermis. What is the most common form of this disorder and how does it present?
Lichen planus
Presents with irregular sawtooth acanthosis and basal damage with the appearance of cytoid bodies
Inflammatory condition that can affect skin, hair, nails and mucous membranes. If affecting the skin, Lichen Planus appears as purplish, often itchy, flat-topped bumps appearing over several weeks
How do immunobullous disorders primarily present? What are some important examples?
Blisters are the primary feature
Important examples:
- pemphigus
- bullous pemphigoid
- dermatitis herpetiformis
Give a brief definition of pemphigus.
What is the most common type?
Rare autoimmune bullous disease
Loss of integrity of epidermal adhesion - affects the DEJ
Variable severity (occasionally fatal), and responds to steroids
Like in other lichenoid disorders, the mucosa of the mouth and respiratory tract may be affected, which in some cases can prove to be fatal.
4 subtypes which are distinguished clinically and histologically. Most common type is Pemphigus vulgaris
In pemphigus vulgaris, what do the auto-antibodies target? What type of immunoglobulin are they? What does this result in?
IgG autoantibodies are made against desmoglein-3
DG-3 maintains desmosomal attachments. Immune complexes form on the cell surface, resulting in complement activation and protease release and subsequent disruption of desmosomes.
The end result is acantholysis (loss of intercellular connections, this is absent in bullous pemphigoid) and the appearance of shallow lesions
In contrast to pemphigus vulgaris, what do the autoantibodies target in Bullous Pemphigoid? How does this present?
Autoantibodies target the hemidesmosomes and basement membrane
This results in local complement activation and tissue damage, and the formation of subepidermal blisters
There is no evidence of acantholysis
When suspecting Bullous Pemphigoid, why is it better to send early lesions for histological analysis, rather than older ones?
Older lesions of pemphigoid show re-epithelialisation of their floor, mimicking pemphigus vulgaris
Give a brief description of dermatitis herpetiformis. What is the hallmark symptom?
What HLA haplotype is it associated with, and what other autoimmune condition does it have a strong association with?
Relatively rare autoimmune bullous disease
Results in intensly itchy symmetrical lesions on the elbows, knees and buttocks. Hallmark symptom is papillary dermal microabscesses, often excoriated.
Associated with HLA-DQ2
Strongly associated with Coeliac disease
What sensitivity do 90% of people with dermatitis herpetiformis have?
What type of immunoglobulins feature in DH and what do they target?
Gluten sensitivity enteropathy
IgA anitbodies target the gliadin component of gluten, but also cross react with connective tissue matrix proteins
Briefly, how does Acne (acne vulgaris) occur, and where does it commonly present?
Increased androgens at puberty, and possible increased androgen sensitivity of sebaceous glands?
Keratin plugs up the pilo-sebaceous unit, which then become infected with the anaerobic bacterium Corynebacterium acnes as they cannot clear the microorganism
Commonly presents in sites with increased sebaceous activity - face, upper back, upper chest etc.
Give a brief description of Rosacea
Common, 10% prevalence in caucasian adults
More common in females
Presents with recurrent facial flushing, visible blood vessels, pustules and thickening of the skin (rhinophyma)
Unlike acne, there are no blackheads/whiteheads (comedones)
Aggrivated by a range of triggers, including…
- sunlight
- alcohol
- spicy foods
- stress
- tetracyclines in some (?)
Name some competitive bacterial flora
- Staphylococcus epidermidis*
- Corynebacterium sp.*
- Propionibacterium sp.*
What test is used to differentiate between Staph aureus and other forms of Staph?
The coagulase test
Staph aureus is coagulase positive and gives off a golden colour
All other forms of Staph are coagulase negative
- Staphylococcus* appear as chains/clusters
- Streptococcus* appear as chains/clusters
Strep = chains
Staph = clusters
How is Streptococcus sub-divided? What are the sub-groups?
Based on haemolysis
Alpha haemolysis - Strep. pneumoniae (pneumonia), Strep. viridans (commensal, endocarditis)
Beta haemolysis - Group A Strep (throat, skin infections), Group B Strep (neonatal meningitis), Group C, G
Non-haemolytic - Enterococcus (gut commensal)
What is the antibiotic of choice for treating a Staph aureus infection?
FLUCLOXACILLIN!!!