Week 2 Flashcards

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1
Q

What are the two types of fascia and how do they differ?

A

Superficial fascia, made up of loose connective tissue and fat

Deep fascia - a tough sheet, dividing regions into compartments

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2
Q

Describe the arterial supply of the upper limb, proximal to distal

A

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)

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3
Q

Describe the venous blood supply of the upper limb, distally to proximally

A

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

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4
Q

How do venous ulcers occur?

Where is the most common site?

A

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

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5
Q

What are some of the chemical mediators of itch in the skin?

A

Histamine

PGE2

Acetylcholine

Serotonin

Kallikrein

IL-2

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6
Q

What are the four categories of causes of itch?

A

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

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7
Q

Systemic diseases associated with itch mostly are neurogenic causes of pruritus. Give some examples

A

Haematological

Paraneoplastic

Liver and bile duct

Psychogenic disease

Kidney disease

Thyroid disease

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8
Q

What are some of the treatments used in the management of itch?

A

Sedative anti-histamines

Emollients

Antidepressants

Phototherapy

Opiate antagonists e.g. ondansetron

(if neuropathic, anti-epileptics)

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9
Q

Where are melanocytes found? What is their function?

A

At the DE junction, in the basal layer

Melanocytes synthesise melanin, and transfer the pigment to keratinocytes via dendritic processes

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10
Q

What type of collagen makes up the dermis?

A

Matrix of Type I and Type 111 collagen fibres

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11
Q

What do the following terms mean:

Parakeratosis

Hyperkeratosis

Acanthosis

Papillomatosis

Spongiosis?

A

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

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12
Q

Give a brief definition of Psoriasis

A

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

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13
Q

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?

A

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

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14
Q

How do immunobullous disorders primarily present? What are some important examples?

A

Blisters are the primary feature

Important examples:

  • pemphigus
  • bullous pemphigoid
  • dermatitis herpetiformis
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15
Q

Give a brief definition of pemphigus.

What is the most common type?

A

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

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16
Q

In pemphigus vulgaris, what do the auto-antibodies target? What type of immunoglobulin are they? What does this result in?

A

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

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17
Q

In contrast to pemphigus vulgaris, what do the autoantibodies target in Bullous Pemphigoid? How does this present?

A

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

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18
Q

When suspecting Bullous Pemphigoid, why is it better to send early lesions for histological analysis, rather than older ones?

A

Older lesions of pemphigoid show re-epithelialisation of their floor, mimicking pemphigus vulgaris

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19
Q

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?

A

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

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20
Q

What sensitivity do 90% of people with dermatitis herpetiformis have?

What type of immunoglobulins feature in DH and what do they target?

A

Gluten sensitivity enteropathy

IgA anitbodies target the gliadin component of gluten, but also cross react with connective tissue matrix proteins

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21
Q

Briefly, how does Acne (acne vulgaris) occur, and where does it commonly present?

A

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.

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22
Q

Give a brief description of Rosacea

A

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 (?)
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23
Q

Name some competitive bacterial flora

A
  • Staphylococcus epidermidis*
  • Corynebacterium sp.*
  • Propionibacterium sp.*
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24
Q

What test is used to differentiate between Staph aureus and other forms of Staph?

A

The coagulase test

Staph aureus is coagulase positive and gives off a golden colour

All other forms of Staph are coagulase negative

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25
Q
  • Staphylococcus* appear as chains/clusters
  • Streptococcus* appear as chains/clusters
A

Strep = chains

Staph = clusters

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26
Q

How is Streptococcus sub-divided? What are the sub-groups?

A

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)

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27
Q

What is the antibiotic of choice for treating a Staph aureus infection?

A

FLUCLOXACILLIN!!!

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28
Q

Some strains of Staph aureus produce toxins - name some of these toxins

A

Enterotoxin

PVL

SSSST

29
Q

What would you use to treat Methicillin-Resistant Staph. aureus?

A

Not fluclox!

Doxycycline

Co-trimoxazole

Clindamycin

Vancomycin

30
Q

What bacterium may cause infection in prosthetic implants? E.g. artificial joints, heart valves IV catheters etc.

A

Staph. epidermidis

31
Q

Name one of the toxins produced by Beta-haemolytic Strep. that damages tissue

A

Beta-haemolytic Strep.

Haemolysin is produced.

32
Q

What are the two most important members of the alpha-haemolytic Strep group?

A

Strep. pneumoniae - most common cause of pneumonia

Strep. viridans - commensal, associated with endocarditis

33
Q

Strep. pyogenes is a Group A beta-haemolytic Strep. Name some of the conditions it can cause.

What is the treatment?

A

Infected eczema

Impetigo

Cellulitis (and Erysipelas)

Necrotising fasciitis

Treatment is with penicillin, as with Staph (Flucloxacillin can be used here too!)

If Necrotising fasciitis, urgent surgical debridement is also required

34
Q

What are the two types of Necrotising fasciitis?

A

Type I - mixed anaerobes and coliforms, usually occurs following abdominal surgery

Type II - caused by Group A Strep

35
Q

When would you swab a leg ulcer?

A

Only if there are signs of cellulitis or infection. Leg ulcers are usually due to a vascular issue

36
Q

What fungal infection is ‘Tinea’ the name for? Where are the following…

  • Tinea capitis
  • Tinea barbae
  • Tinea manuum
  • Tinea unguium
  • Tinea cruris?
A

Tinea = ringworm

Capitis = scalp

Barbae = beard

Manuum = hand

Unguium = nails

Cruris = groin

37
Q

What are the 3 most common causal organisms of ringworm infection? (Dermatophytes)

How is infection diagnosed?

A
  • Trychophyton rubrum* - by far the most common, roughly 70%
  • Trychophyton mentagraphytes*
  • Microsporum canis*

Diagnosed by taking a skin scraping and sending to the lab for culture and microscopy

38
Q

How are Dermatophyte infections treated?

A

Small areas of skin/nails - Clotrimazole (Canestan) cream

Extensive skin infections/scalp infections - either Terbinafine or Itraconazole, both given orally

39
Q

What is the causative organism in Scabies infections? What is the treatment?

A

Sarcoptes scabiei

Incubation period of up to 6 weeks and causes an intensly itchy rash affecting finger webs, wrists and genital area

Treatment - malathion lotion applied overnight, or benzyl benzoate

40
Q

What is the fancy word for ‘lice’? What is the treatment?

A

Pediculus e.g. Pediculus capitis (head lice)

Treatment is Malathion lotion

41
Q

Why can gram positive organisms survive in the environment?

A

Because of their cell walls

42
Q

What is the causative organism of both chickenpox and shingles?

A

Varicella zoster

Varicella causes chickenpox

Herpes zoster causes shingles

43
Q

What are some of the complications of chickenpox?

A

Secondary bacterial infection

Pneumonitis

Haemorrhagic complications

Encephalitis

Scarring

44
Q

What are some of the features of Shingles?

A

Reactivation of the varicella zoster virus later in life

Follows a dermatomal distribution

Appears in the elderly and the immunocompromised

Progression goes tingling/pain > erythaema > vesicles > crusts

Pain increases with age, and is neuralgic in nature

45
Q

If Shingles presents on the face and affects one of the eyes, what is the name given to this condition?

A

Opthalmic zoster - opthalmic branch of the trigeminal nerve is affected

46
Q

What are the features of Ramsay-Hunt Syndrome?

A

Vesicles and pain in the auditory canal and throat

Facial palsy (CN VII)

Irritation of CNVIII - presents as deafness, tinnitus, or vertigo

47
Q

Describe the pattern of disease of Herpes Simplex

A

Presents initially in pre-schoolers as extensive ulceration in and around the mouth. Lasts for about a week.

Can recur in later life with blistering around the mouth and can be spread.

Two types:

  • HSV Type I, main cause of oral lesions and causes half of genital herpes. Can also cause encephalitis
  • HSV Type II - rare cause of oral lesions, and can also cause genital herpes and encephalitis
48
Q

What anti-viral drug can be used for both varicella zoster and herpes simplex? How does it work?

A

Aciclovir

Analogue of guanosine, is selectively taken up into viral DNA and inhibits replication.

Doesn’t eliminate latent virus

49
Q

Briefly describe molluscum contagiosum.

How is it treated?

A

Causes the formation of fleshy, firm, pearlescent nodules

Self-limiting, but may take months to disappear

Common in children but can also be sexually transmitted

Can be treated with liquid nitrogen therapy

50
Q

What virus causes warts? How is it treated?

What other diseases can this virus cause?

A

Human papilloma virus - self-limiting and uncomplicated, most commonly seen in children.

Treated with topical salicylic acid

Over 80 types of HPV, 1-4 are most common in warts/verrucas

Also causes genital warts - HPV 6 and 11

Associated with cervical cancer - HPV 16 and 18

Can also cause head and neck cancer

51
Q

What is the other name for “slapped cheek” disease? What is the causative organism?

How else can this affect the body?

A

Erythema infectiosum

Caused by parvovirus B19

Can also cause acute arthritis, especially in the wrists

52
Q

What animal is Orf associated with? Who gets it? Is it serious?

A

Orf is associated with sheep

Farmers, typically

No, self-limiting and constitutional symptoms are rare

Appears as a firm, fleshy nodule on the hand

53
Q

What is the causative organism of syphilis? How is it transmitted and treated?

What are the three stages of presentation?

A

Treponema pallidum

Transmitted via sexual intercourse

Treated with a series of injections with penicillin

Primary stage - painless ulcer at site of entry

Secondary stage - red rash over body, prominent on soles of feet and palms

Tertiary - CNS, cardiovascular, gummatous etc. complications

54
Q

Lyme Disease: causative organism, features at presentation and treatment

A

Organism - Borrelia burgdorferi

Features - erythema migrans (early), heart block, nerve palsies, arthritis (late)

Treatment - doxycycline or amoxicillin

55
Q

Briefly describe the immunopathology of allergic contact dermatitis

A

Antigen is processed in the epidermis by Langerhan’s cells

Antigen is then presented to Th cells in the dermis, which migrate to nodes via the lymphatics

56
Q

How is a contact allergy diagnosed?

A

Via patch testing

57
Q

What is the difference between contact allergic dermatitis and irritant (contact) dermatitis? (kind of obvious…)

A

Irritant dermatitis is a non-specific reaction in response to physical irritation rather than a specific allergic reaction.

The two may be different to distinguish between, and may also co-exist

58
Q

Give a brief description of eczema (atopic dermatitis).

What % of school children does it affect?

A

Ill-defined erythema and scaling

Generalised dry skin

Appears in areas of flexion

Associated with other atopic disease e.g. asthma, allergic rhinitis, food allergies etc.

Affects up to 25% of school-aged children

59
Q

Secondary infection with eczema is common. If crusting appears, what organism is this indicative of?

A

Staph. aureus

60
Q

What other secondary infection is associated with eczema and classically appears as monomorphic punched out lesions? (see picture)

A

Eczema herpeticum, caused by secondary infection with the Herpes Simplex Virus

61
Q

The UK diagnostic criteria for eczema consists of itching plus 3 or more further features. Name some of these features

A

Visible flexural rash

History of flexural rash

Personal history of atopy

Generally dry skin

Onset before the age of 2

62
Q

What treatment options are available for eczema?

A

Emollients

Avoidance of irritants (soaps, shower gels etc.)

Topical steroids

Treating secondary infections

Phototherapy - mainly UVB

Systemic immunosuppressants

(Biologic agents are also an option)

63
Q

What causes atopic eczema? What has been identified as the most important genetic component?

A

Multiple genetic and environmental factors contribute to eczema development

Most important component is filaggrin, encoded for by thew FLG gene

64
Q

What form of eczema is commonly mistaken for psoriasis? How are the two differentiated?

A

Discoid eczema

Eczema crucially does not form raised plaques, unlike psoriasis

65
Q

Name the type of eczema

What is the clue?

A

Photosensitive eczema (Chronic Actinic Dermatitis)

Collar cut-off

66
Q

What term is given to inherited genetic skin conidtions?

What common genetic skin condition may present as infantile seizures?

A

Genodermatoses

Tuberous sclerosis is a genodermatosis that may present as infantile seizures

67
Q

What is the earliest cutaneous sign of tuberous sclerosis, pictured here?

A

Ash-leaf macule

68
Q

Tuberous sclerosis is characterised by the formation of numerous benign tumours.

Where might these tumours present?

A

Peri-ungual fibromas - around nails

Facial angiofibromas - often misdiagnosed as acne

Cortical tubers and/or calcification of falx cerebri - tumours in the brain, may cause seizures

Hamartomas = angiomyolipomas which may present in the heart, lung or kidneys

Bone cysts

69
Q

Mutations in what genes can result in tuberous sclerosis? What do these encode for?

What is the inheritance pattern?

A

Mutations in either TSC1 or TSC2

These encode for tuberin and hamartin

Autosomal dominant