Other- ENT, derm, gero Flashcards

1
Q

What is ageing

A

=Gradual development of changes in structure and function that are not due to preventable disease or trauma
-Associated with decreased functional capacity (reduced muscle, cardio-resp reserve, cognitive capacity, bladder capacity)
- increased probability of death
-Reduced homeostatic reserve and become more frail: more at risk of severe deterioration from minor insult, poorer recovery and resilience
-less independence

Old age >65 years old

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2
Q

Difference between 1) impairment, 2) disability and 3) handicap. And examples of solutions for these

A

-the physical damage caused by the disease process (e.g. Paralyzed left arm from stroke=physio strengthening exercises)
-the tasks that cannot be performed as a result of the impairment (e.g. Unable to get dressed properly due to paralyzed arm= aids and appliances to help
–how it affects the individual’s lifestyle (e.g. Lost ability to enjoy hobbies, loneliness =carers, social activities

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3
Q

The Geriatric giants (6 Is)

A

-Instability – falling easier
-Immobility – unable to walk
-Incontinence = peeing/ pooing uncontrollably
-Intellectual impairment – dementia, delirium
-Isolation - loneliness
-Iatrogenesis – medically induced problems

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4
Q

What is age discrimination and give examples

A

-Demeaning Attitudes, language and behavior for older people
-Prioritising younger people for services (eg for cateracts or hip surgery as it limits them more because of their job)
-Age-restriction of services or procedures i.e. SEDATION
-Lack of accessibility – transport, lifts, ramps
-Neglect/Physical/ emotional/ financial/ sexual abuse

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5
Q

Reasons for poor compliance for old people taking their meds and ways to overcome

A

-Poor explanation by doctor
-Side effects
-No noticeable benefit
-Scared by package insert
-Poor mental function – cannot remember
-Poor physical function – manual dexterity, vision (cannot read small print)

-Explain things carefully, leaflets, speak to carer or relative, communicate with GP, dosing boxes, supervision by carers

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6
Q

How drug action differs in old patients

A

-Different pharmacokinetics=reduced GI absorption, reduced excretion in liver/kidney, altered protein binding, increased sensitivity of drugs
-Altered drug action
-Drug interactions= polypharamcy, co-morbidities
-Adverse effects =increased sensitivity to side effects

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7
Q

Common side effects in old people of opioids, clindamycin, sedatives, NSAIDs, anticholinergics

A

-Opioids – constipation and confusion
-clindamycin/ clarithromycin- diarrhea
-Sedatives – confusion & falls
-NSAIDs – peptic ulceration, fluid retention, renal impairment
-Anticholinergic – CONFUSION, CONSTIPATION, URINE RETENTION, BLURRED VISION & DRY MOUTH

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8
Q

How central nervous system changes with old age

A

-neurones lost as you age=reduced coordination, slower reaction time, reduced learning
-increased amyloid protein deposition=poorer short term memory
-decreased dopamine =parkinson’s, depression
-confusion
-altered taste, smell

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9
Q

Changes in the cardiovascular system that occur with ageing

A

-Vascular changes: Atherosclerosis – hypertension - stroke
-Reduced baroreceptor response =postural hypotension
-Pathology - need artificial valves, transplants
-reduced nitric oxide=delayed angiogenesis
- thickening of heart ventricles as heart has to pump at higher force
-Reduced cardiac function
-Cardiac conductive system: arrhythmia, lower max HR
-Increased systolic blood pressure (but diastolic remains stable)

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10
Q

How the following hormones change with age and their effects: 1)melatonin, 2) dopamine, 3) thyroxine, 4) PTH, 5) insulin, 6) aldosterone

A

1) decreases -sleep disturbances
2) decreases - parkinson’s, depression
3) decreases- lower core temp, reduced metabolic rate, fatigue, constipation
4) high- more Ca in blood causing reduced bone density
5) decreases- increased diabetic risk
6) decreases-drop in blood pressure - postural hypotension

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11
Q

Changes in eyes with ageing

A

-Anatomical changes around eyelids
-decreased tear production and drainage
-Presbyopia -dense less flexible lens = inability to focus on nearby objects
-Ophthalmic dysfunction: retinopathy, macular degeneration, cataracts, glaucoma
-Pupillary diameter decreases and ability for diameter to change reduces- night vision problems

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12
Q

Hearing changes that occur with ageing

A

-Loss of hair cells and cochlear neurons
-Impaired conduction and amplification = Conductive hearing loss
-Reduced ear wax=increased risk of infection
-Pressure imbalance in middle ear
-Presbycusis -age-related hearing loss
-Inability to hear high frequencies, struggle with background noise
-Loss of balance, dizziness
-Tinnitus

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13
Q

Respiratory changes that occur in ageing

A

-reduced volume of rib cage, reduced muscle strength
-Reduced coughing reflex =higher risk of infection and choking.
-Breakdown of alveolar structure and its elasticity (emphysema and COPD)
-Diminished aerobic capacity
-Aspiration: due to reduced ciliary escalator, dementia, being fed by tubes

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14
Q

GIT changes that occur with ageing. Why peptic ulcers are common

A

-Reduced apatite
-Altered gastric and oesophageal motility=reflux, dysphagia, heart burn
-Reduced goblet cells so less mucin, and decreased bicarbonate: affects bioavailability of drugs, peptic ulcers
-Reduced drug absorption
-Altered hepatic / renal function and hence drug metabolism
-Artificial bits and transplants

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15
Q

Skin changes that occur with ageing (intrinsic and extrinsic)

A

-Intrinsic: reduced fibroblasts and collagen=fine wrinkles, pale, less elastic, dry, smooth, thinner
-Extrinsic: smoking, UV, diet= deep wrinkles, rough, pigmentation, lost elasticity

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16
Q

Musculoskeletal changes during ageing

A

-Reduced protein synthesis, muscle growth, ability to repair
-Reduced size and number of muscle fibres
-Replacement of active muscle fibres by collagen-rich non-contractile fibrous tissue
-Reduced muscle mass associated with changes in hormone levels
-Reduced Flexibility - due to reduction in cartilage
-Reduced motor neurones
-Increased fat deposition at the expense of lean muscle
-Less efficient metabolism particularly in fast-twitch fibres – reduced blood flow
-Decreased vitamin D and blood calcium = decreased bone density = increased risk of fracture, osteoarthritis, joint changes, osteoporosis

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17
Q

How saliva changes with ageing

A

-reduced stimulated and unstimulated salivary flow
-Modest decrease in the concentration of mucins and some saliva electrolytes.
-decreased antimicrobial factors
-due to reduced salivary gland function, medication, disease

-wake up with dry mouth, feels dry a lot of the time, takes sips of water when chewing and speaking

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18
Q

Types of medications and diseases that cause Xerostomia

A

-Anti-cholinergic
-ACEI
-Diuretics
-Ca channel blockers
-b-adrenergic blockers
-chemo and radiotherapy
-Carbemazepine
-antidepressants
-anxiolytics
-antiparkisnonians

-Sjögren’s syndrome
-Diabetes
-Dehydration

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19
Q

Changes that occur to our teeth and mucosa with ageing

A

-Enamel: thinner, darker, reduced translucency, cracks
-Darker: dentine showing through, staining, less water content (can cause cracking), sclerosis (tubule occlusion), tertiary dentine
-Pulp: smaller, calcifications, reduced space (tertiary dentine), degeneration of pulpal neurons, more fibrous, less cellular
-Cementum: thicker, widening of the major apical foramen, decreased vascularity, more fibrous, decreased cellularity, non-patent canals
-Physiological and pathological TSL
-Periodontium: more fibrous, less cellular, less proteoglycans/protein/collagen, little attachment loss, buccal recession
-Mucosa: reduced microvasculature, delayed wound healing, less elastic

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20
Q

Anatomy of the external, middle and internal ear

A

-External =pinna, external auditory meatus, auditory canal, tympanic membrane
-Middle=conduction of sound by the ossicles- Incus, malieus, stapes. Petrous part of temporal bone. Eustachian tube
-Inner =labyrinth- vestibule and cochlea. Deepest part of petrous temporal bone. Balance

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21
Q

What is conductive and sensory deafness. Types of tests to assess it

A

-Conductive deafness – air not transported through the ear = usually due to wax
-Sensory neural deafness – due to CNVIII (vestibulocochlear), inner ear hair cell damage, brain processing

-Tune fork tests: Rinne and Weber
-Pure tone audiometry
-Electric response audiometry

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22
Q

Explain the Rinne test. Does it test conductive or sensory hearing deafness

A

-A tune fork test to assess conductive hearing.
-Compares air and bone conduction
-Hit fork against object, place on mastoid process (BC) and compare this to 3cm in front of ear (AC)
-Normally: AC better than BC
-Conductive deafness: BC>AC

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23
Q

Explain the Weber test. Does it investigate conductive or sensory hearing deafness

A

Investigates if it is conductive or sensory
-Tune fork put in middle of back of head and ask which side patient hears the sound
-If louder in deaf ear= conductive
-If louder in normal ear=sensory

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24
Q

What is 1) pure tone and 2) electric response audiometry. When are they used

A

1) Exposed to a range of sounds with varying decibels. In soundproof booth and special headphones
-Both air and bone conduction tested
-If abnormality of Rinne’s or Weber’s test
-Subjective

2) Used in patients/children that you can’t get a reliable answer from
-Objective score for somebody’s hearing

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25
Q

What is otitis external. Causes, symptoms, treatment

A

-inflammation of external ear
-Infection, Irritants, skin disorders, trauma, otitis media spreading outwards
-very painful with serous discharge. Inflamed red ear drum. Blockage.
-Tx- GENTAMICIN & STEROID (OTIMIDE) EAR DROPS. ANTI-FUNGAL if fungal infection

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26
Q

What is Perichondritis. Causes and symptoms

A

-Inflammation of the perichondrium- connective tissue which surround cartilage of the external ear
-can be due to auricular haematoma due to trauma (multiple haematomas can cause cauliflower ear)

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27
Q

Types of benign and malignant external ear neoplasms

A

1) Benign
-osteoma -bony overgrowth
-Ceruminoid adenoma - wax glands

2) Malignant
-Basal cell carcinoma
-SCC
-Ceruminous adenocarcinoma

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28
Q

What is acute Otitis media: symptoms, cause, tx, complications

A

-Infection of middle ear usually in childhood (<5)
-Blockage of underdeveloped Eustachian tube so secretion from middle ear to pharynx get infected
-painful, discharge, fever, or may be oblivious

-Complications: otitis external, scarring if recurrent, perforation, mastoiditis, intracranial spread
-Progression to chronic otitis media with effusion (GLUE EAR) where fluid builds up, prone to infection. Conductive hearing loss

-Tx=Antipyretics, antibiotics, decongestants, surgery

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29
Q

What is acoustic neuroma. Symptoms

A

-Benign tumour of the VESTIBULOCHCOLEAR nerve in cerebellum pons
-doesn’t take much enlargement to cause problems
-unilateral deafness, vertigo, unsteadiness, facial palsy

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30
Q

What is benign paroxysmal positional vertigo. Symptoms

A

-causes 20% of dizziness. Triggered by different head positions (lying down, looking up)
-age related or post head injury
-Sudden recurrent episodes <1 hour: world feels like its spinning, feel sick, no vomitting, disorientation
-conservative management, surgery rare

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31
Q

What is cataracts. Causes

A

-opacification of the eye lens (cloudy)
-Slowly progressive
-Over iris so lose visual clarity
-Causes: Age, trauma, too many CT scans, radiation, infection

32
Q

Haemorrhages on retina may suggest what systemic diseases

A

uncontrolled diabetes mellitus
high BP

33
Q

What is visual acuity and how to record a VA score

A
  • how easily you can see things at a distance. clarity or sharpness of vision
    -Snellen test: measured 6 metres from the chart, one eye at a time. Comparing how a normal person should see. Eg. 6/12 means that you can see, at 6 metres, what a ‘normal’ person can see at 12 metres from the chart.
34
Q

Different causes of red eye

A

a manifestation of sight-threatening conditions
-conjunctivits, acute glaucoma, uveitis, corneal ulcer

35
Q

What is glaucoma. symptoms

A

-increased intraocular pressure causing damage to ocular nerve
-painful or painless
-red eye, loss of visual acuity, sight threatening, white sclera, dilated pupil

36
Q

What is Macular degeneration

A

Causes: age, family history

-Degeneration of macula at back of eye where image is concentrated
-Loss of central vision e.g. can only see round the outside
-blood vessels from choroid can leak exudate and haemorrhage

37
Q

Likely diagnosis if someone has constant headache, unilateral enlarged temporal artery and tender, reduced visual acuity, jaw pain when eating

A

Temporal arteritis

38
Q

Investigations and treatment for temporal arteritis

A

-ESR 90 and CRP 20 increased
-Temporal artery biopsy – inflammatory and giant cells
-Ultrasound scan = decreased size of lumen

Tx: Admitted to hospital as sight threatening
-500mg IV steroids daily for 3 days, followed by tapering dose of oral steroids for 2 years

39
Q

A systemic disease that presents with mouth ulcers and red eye

A

-Behçet’s disease

40
Q

Systemic diseases that causes eye problems

A

-IBD (uveitis)
-Behcet’s (red eye)
-Pemphigus and pemphigoid (conjunctivitis, lesions)
-Steven Johnson (blistering)
-Sjogren’s (dry)

41
Q

Blow out fractures: cause, symptoms, who to refer to

A

-orbital floor injury. Contents pushed back, globe not ruptured
-Associated with fractured zygomas
-Test eye movement and pupil response- Eyes don’t move together
-Subconjunctiva haemorrhage –very red sclera
-Prolapse orbital contents into maxillary sinus
-Diplopia = double vision
-Hypoglobus – inferior displacement of globe in the orbit
-Infraorbital anaesthesia/ numbness
-Enophthalmos – posterior displacement of the eyeball within the orbit (due to changes in volume)

A&E then if Eye socket – maxillofacial surgeon
Eyeball – Ophthalmology

42
Q

What is orbital cellulitis. Causes. Symptoms

A

-bacterial infection, either by direct trauma or infection that spreads from the sinuses or tooth
-Inflammation around eye and Proptosis – eye sticks out. Restricted eye movement
-Fever
-Treatment = Sinus drainage + IV antibiotics. Sub periosteal abscess

43
Q

What is Ramsay Hunt syndrome

A

Herpes Zoster reactivation
Lays dormant in the geniculate ganglion
Causes ipsilateral facial nerve palsy
Can’t close eye properly.
Risk of hyperkeratotic eye
Treatment: IV Acyclovir

44
Q

Eye and ear conditions that can lead to facial palsy

A

Cholesteatoma (middle ear)
Acoustic Neuroma (benign inner ear tumour)
Keratitis (inflamed cornea)
Herpes Zoster reactivation (Ramsay Hunt)

45
Q

How does the body compensate an increase in intra-cranial pressure

A
  1. Decreasing the production of CSF
  2. Restricting the blood flow to the brain (by vasoconstriction)
46
Q

Initial management of a scalp injury

A

-Scalp has a very good blood supply so injury may bleed profusely = vessels don’t shut down due to MUSCLE PULL
-Control bleeding with direct pressure
-But do not apply pressure when there is possible underlying skull injury

47
Q

Signs of brain injuries and therefore need referring to A&E

A

-Headache
-Dizziness
-Confusion, Feeling dazed
-Sensitivity to light
-Nausea/vomiting
-Difficulty remembering incident- amnesia
-Numbness/tingling/neck stiffness
-Blurred vision
-Loss of consciousness
-CSF leakage (straw coloured, high glucose content)

48
Q

Difference between primary and secondary brain injuries

A

1) Diffuse axonal injuries. Brain damage occurs at time of insult due to direct damage to brain. Irreversible as damage is already done. Coma or death
2) Indirect. Damage Occurs after initial insult, progressive increase in intracranial pressure and/or brain herniation through Forman magnum. eg. Extra-dural haematoma.

49
Q

Explain 1) concussion, 2) contusion, 3) uncal herniation during brain injuries

A

1) transient alteration in neurological function. Usually no detectable brain damage. May have brief loss of consciousness. Headache, grogginess, short term memory loss
2) Bruised brain. Brain hits against skull. Unconscious or. decreased consciousness
3) A bleed or mass increases intracranial pressure, displacing the uncus

50
Q

Explain Sub dural, extra dural and subarachnoid haematoma (venous/arterial, quick/slow onset, appearance on MRI)

A

-Caused by intracranial bleeding. A collection of blood within tissue

Sub-dural haematoma: blood collection between brain and dura. Venous bleed. Slow onset. Can be mistaken for dementia. Crescent shape on MRI as can cross suture
-Extra-dural haematoma: blood collection between dura and the skull. Middle meningeal artery. Quick onset within a few hours. Common in blow to the head. Convex on MRI as cannot cross sutures
-Subarachnoid Haemorrhage: bleed beneath arachnoid membrane due to cerebral aneurysms. Eg Berry aneurysm
-Intracerebral haematoma: blood collection within the brain

51
Q

Initial management of head injuries

A

ABCDE
Neurological evaluation -ACVPU, GCS
Radiological evaluation-CT
Treat intracranial pressure

52
Q

Explain the ACVPU assessment

A

Rapid method of assessing someones level of consciousness. Can calculating their early warning score (NEWS2) alongside their basic observations (vital signs).
-A Alert
-C New onset confusion
-V Verbal response (talk to them)
-P Pain response (painful stimulus)
-U Unresponsive

53
Q

Explain the Glasgow coma scale

A

-Assesses patient’s neurological condition. More in-depth than ACVPU
-Value range 3 to 15, 15 being full alert, 3 being in a coma
-Assessing patient’s response to stimuli: Testing eye, motor and verbal responses
-According to the score it classes brain injuries as mild (13-15), moderate (9-12) or severe (3-8)

54
Q

What Glasgow coma score is the threshold for intubating a patient

A

8 (anything 3-8)
As cannot control their own airway

55
Q

Treatment of intracranial haematomas

A

-Epidural & Subdural: Craniotomy for evacuation of the bleed
-Intra-parenchymal: No surgery
-Treat increased ICP medically:
Iv fluids
Hyperventilation
Mannitol
Hypertonic saline
Anticonvulsants

-increasing BP and slowing HR

56
Q

Early and severe signs of intracranial haemorrhage

A

early= severe headache, dizzy, nausea, unequal pupil size, sleepy
Severe= deteriorating consciousness, rigid neck, slow pulse, slow RR, convulsions

57
Q

What to ask a patient if suspect a brain injury

A

-Were you knocked out? How long for
-What can you remember about the incident?
-What’s the last thing they remember before they lost consciousness?
-What’s the first thing they remember on waking up?
-Any witnesses
-Vomitting, blurred vision, Headache, Dizziness, Confusion, Sensitivity to light, Numbness

58
Q

Difference between anterograde and retrograde amnesia

A

-ANTEROGRADE = people can’t form memories after the event (post-traumatic)
-RETROGRADE amnesia = can’t remember events leading up to the event

59
Q

Systemic response to burns when 20% of Toal body surface area is affected

A

-Hypovolemia due to intravascular fluid leaking into the interstitial space causing interstitial oedema
-reduced heart contraction
-increased systemic vascular resistance (peripheral vasoconstriction) due to hypovolemia
-Bronchonstriction.
-Muscle wasting. Hypocalcaemia.
-Depression of immune response
-Burns are clean wounds but can quickly be colonised by bacteria – can cause sepsis

60
Q

Explain 1st to 4th degree burns

A

1) Epidermis. Dry, painful, no blistering or scarring (eg. sunburn)
2) Epidermis and partial thickness of dermis. Wet, painful, blistering, no scarring (eg. scalding)
3) Epidermis and full thickness dermis. Dry, insenate, scarring. (eg. flame)
4) Involves underlying subcutaneous tissue, tendon or bone. White, charred, painless, significant scarring

61
Q

Management of burns

A

ABCDE
Immediate management- First Aid:
-Stop the burning process
-Remove clothing
-Cool the burn – lukewarm water for 20 minutes
-Keep the patient warm
-Cover with clingfilm
-Relieve pain – simple analgesia
Definitive treatment:
-Surgery: eg. excision with skin grafting, escharotomy for some full-thickness burns

62
Q

Causes of undernutrition

A

-not eating enough
-exercising lots
-diarrhoea, vomitting
-increased body temp due to infection
-Painful mouth, poor dentition, impaired mastication
-Swallowing difficulties, Xerostomia
-Reduced taste and smell
-Unable to cook
-Side effects of medication
-Frequent medical intervention
-Poverty, lack of access to food
-Wrong nutritional advice
-Poor digestion and absorption
-lost appetite

63
Q

Definition of undernutrition. What is the BMI

A

Eithers:
-BMI <18.5 kg/m2
-Unintentional loss of 10% body weight over 3-6 months
-BMI of 20 AND unintentional loss of >5% body weight over last 3-6 months

64
Q

List methods of nutritional support

A

-Food fortification to increase nutritional value, energy, protein
-Oral supplements (powders, shakes)
-Enteral- feeding through tube
-Parenteral-IV

65
Q

Rashes made worse and better with sun

A

-better: eczema, psoriasis
-worse: lupus

66
Q

Explain these terms for describing lesions: hive, macule, patch, papule, nodule, plaque, crust, scale, ichthyosis, vesicle, bulla, pustule, erosion, ulcer, excoriation

A

-Hive – dermal pathology (skin smooth but surface raised)
-Macule – little and flat
-Patch - big and flat
-Papule – little and raised <1cm
-Nodule – big and raised >1cm
-Plaque – big and raised but sticks out less
-Crust – dried pus or blood
-Scale – accumulation of excess keratin. Flakes (yellow/white)
-Ichthyoses = so much keratin on skin begins to crack
-Vesicle- small fluid filled blister <1cm
-Bulla – large fluid filled blister >1cm
-Pustule – filled with pus
-erosion- partial loss of epidermis, heals without scarring
-ulcer-full epidermis and some dermis. Scarring. Crusting, pus, necrotic tissue (slough)
-Excoriation -localised damage due to scratching

67
Q

Which is 1) epidermal and 2) dermal: lichenification and warty process, and scarring/infiltrative process. Give examples of conditions

A

1) Lichenification, wart. Eczema, psoriasis
2) Infiltrative. nettle rash, cellulitis, chicken pox

68
Q

Common skin cancers and their causes. Differences. Risk factors. management options

A

1) Basal cell carcinoma: basal layer of epidermis. slow growing. Rarely metastasis. Most common. Pearly white domes telangiectasia.
2) SCC: Hyperkeratoses. rapid growing, may metastasise via lymph nodes. Common on scalp, pinna, lower lip, dorsal hand
3) Malignant melanoma: Melanocytes. dark weird mole

-radiation, UV, genetics, immunosuppression, skin type
-Tx: excision with clear margins, curettage and cautery, cryotherapy (extreme cold), radiotherapy/ chemo if metastatic, lymph node dissection if high risk, topical therapy,

69
Q

Explain the ABCDE screening for suspected skin cancers

A

-Asymmetry
-Border irregularity
-Colour variation – multiple colours
-Diameter >6mm
-Evolving – changes in size, colour shape over months/years [moles are stable]

70
Q

Contact dermatitis presentation. What type of hypersensitive is it

A

-Type IV T cell mediated reaction
-Causes itchy, inflamed, red skin
-Irritant or allergic: nickel or epoxy resin

71
Q

Difference between these 2 types of eczema: 1) atopic and 2) contact

A

1) Chronic inflammatory condition, excess hypersensivity to multiple trigger in environment such as pollen and dust
2) Reaction to an irritant (repeated hand washing) or an allergic reaction (contact urticaria or allergic contact eczema)

Yellow orange crusting, scaling

72
Q

Type of hypersensitivity and testing of these contact types of eczema: 1) allergic contact dermatitis and 2) contact urticaria, that can be caused by rubber latex gloves

A

1) type IV hypersensitivity (delayed) Patch testing
2) type I hypersensitivity (immediate) Skin prick or RAST testing

73
Q

Do monomers or polymers cause allergic reaction

A

Acrylate monomers: once polymerised should not cause a contact allergen
Polymer is chemically inert so won’t cause any reactions

74
Q

List skin diseases that cause oral manifestations

A

Lichen planus
Lupus
Erythema multiform
Orofacial granulomatosis
Crohn’s
Pemphgus and pemphigoid

75
Q

What is psoriasis. Risk factors

A

-Immune mediated disease. Disorder of keratinisation
-plaques, dryness, scaling
-Risk factors: smoking, obesity, alcohol, vit D deficiency

76
Q

Explain the need for steroid cover for people taking steroids

A

-During surgery, there is increase demand for cortisol to be produced to due to high stress
-Cortisol is made by adrenal gland by release of ACTH from pituitary.
-Those on steroids means their body stops making ACTH and therefore doesn’t produce cortisol
-So need to increase steroid dose because body cannot make enough cortisol to deal with stress.=adrenal insufficiency