week 2 Flashcards
Define the integument and list its main functions
Skin hair and nails
barrier protection (dehydration, infection, injury, solar radiation)
thermoregulation
sensation
repair
vit D production.
Recognize, understand and describe the three main layers of skin, the sub-layers of the epidermis.
epidermis- varies in thickness
basal layer- first single layer of keratinocyters (some stem cells)
stratum spinosum- thickest - living cells differentiating and moving distally. many desmosomes + spines
stratum granulosum- 1-4 rows of cells- prominent granules.
stratum corneum- outer layer. squamous cells- cornified - tough and resistant to injury. nonpolar lipids between cells provide waterproofing.
dermis
hypodermis- pale as lots of fat.
List the main cell types found in each skin layer, and explain the flow of cells in the epidermis
langerhans cells - dendritic antigen presenting cells.
dermis- dense irregular connective tissue. (collagen, not parrallel) mostly fibroblasts cell type.
dermal-epidermal border- wavy to resist shear. has rete ridges, can have dermal papillae.
hypodermis- fascia/ subcutis. made of fat cells.
melanocytes found in basal cells level.
Explain how and where each main function of the integument is performed
vitamin D- made by basal cells requires UV light. converted to active form in the liver (1,25 dihydroxyvitamin D3)
function of hypodermis- insulation cushioning and energy storage.
the dermis facilitates heat exchange.
the epidermis - spinosum layer proliferates cells. Corneum build up causes thickening.
main kind of skin apendages
glands- eccrine sweat glands
sebaceous glands- sebum into hair follecules.
apocrine sweat glands. secrete into hair follicles. armpits and anogenital region- after puberty phermones in some mammals.
hair - acne comes from this.
nails
sense organs- thermoreceptor, meissners corpuscle- light touch
nocicepteor
pacinian corpuscle
List the potential types of environmental ‘insults’ upon the skin
radiation
physical trauma (pressure, burns cuts)
irritants
allergans
microbes/ parasites
Explain how the main insults are resisted by the skin, through its normal structure and components
Explain how skin can adapt to stimuli (such as friction, sunlight, heat) over time
vasoidlation/ vasoconstriction- sweating. increaced blood flow to subpapillary plexus.
hyperkaratosis- callus- thickening of stratum corneum (slow reaction)
tanning- melanocyte response
uv protection- melanocyte increase activity. transmit more. additional protection by epidermal thickening. UV damages DNA- MSH- MC1R Camp stim. transcription.
Describe examples of common abnormal skin conditions that have environmental causes
lichenification- hyperkeratosis (rubbing/ scratching)
contact dermatitis- inflam response to contacting something.
allergic contact dermatitis- immune system involved. tiny amount needed.
irritant contact derm much more common. allergic needs sensitisation.
fungal/ microbe/ parasitic. e.g impetigo. ringworm. cellulitis.HPV.
discuss burns- grading and extent of sensation lost.
discuss sun burn and the skin changes that it can cause
loss of elasticity
polymorphic light eruption
naevi- benign proliferation of melanocytes.
freckles (ephelides) keratinocyte change- some ginetic component.
solar lentigos- age related ‘ liver sports’
solar keratoses-benign growth of keratinacytes.
cancer divided into melanoma and non melanoma skin cancer
Outline the underlying causes of multisystem rheumatic disease
gut biome changes in each person
il-17 secretion for ankylosis
Recognise the heterogeneity of clinical features associated with these mechanisms
big variability in symptoms and cause of symptoms, meaning that single drug treatment regimes are unlikely to work completely.
Recognise that cardiovascular disease is a consequence of these diseases
particular suceptibility to cardiovascular issues with sle, RA etc
vasculitis, pulmonary artery htn, MI. aortic valve deformity.
Outline the use of steroids and non-steroidal anti-inflammatory drugs in relation to joint disease
NSAIDS- 1st line in community for new presentation. long term use avoided due to renal, liver, cardiac issues.
Steroids- fast acting and used in emergency/ serious. most vasculitis. connective tissue disorders. side effects depend on route of administration.
Outline the indications, mechanisms of action and the main adverse drug reactions of disease-modifying anti-rheumatic drugs
inflammatory arthritis and also connective tissue/ other disorders e.g sjorgens SLE.
methotrexate- purine/ pyrimidine synthesis inhibitor. can cause hepatotoxicity. pro-drug. activates after polyglutamation in cells. eliminated by kidneys- nsaids can reduce excretion
increased extracellular concentrations of adenosine- which can be anti inflam.
sulfasazine-
hydroxychloroquine-
Outline the indications, mechanisms of action of the biologics used in rheumatology
prod from living cells.
anti-TNF factors.
2 types- alpha, beta.
proinflamatory cytokine production (il1,6)
anti-tnf bind to tnf (some one, some both) variably cause apoptosis or not of tnf cells. variation in binding in circulating or cell bound TNF.
mechanism of sulfasalazine
hydroxycholoroquine
leflunomide
side effects of Biologics.
Identify important features of the dermatological history
Dermatology examination: use key dermatological terms to describe a rash
macule- less than 1cm
papule- raised macule
nodule- raised greater than 1 cm.
plaques- raised large with flat top.
discuss erythema multiform
what is stevens johnson syndrome and toxic epidermal necrolysis
variants of same condition- depends on body surface area involvement.
