Rheumatology and Dermatology Flashcards

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1
Q

What are some possible modes of treatment for atopic dermatitis (eczema)?

A
  • Calcineurin inhibitors: tacrolismus, pimecrolismus
  • Topical steroids
  • Antibiotics for open lesions
  • Antihistamines
  • Leukotriene inhibitors: montelukast
  • UV light therapy
  • Systemic steroids
  • Immunosuppressive drugs: methotrexate, cyclosporin, azathioprine
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2
Q

How does one diagnose osteoporosis?

A

Bone mineral density test (DEXA: dual energy X-ray absorptiometry): T-score <= 2.5

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3
Q

What are the possible complications of osteoporosis?

A
  • Vertebral crush fractures
    >> Acute back pain
    >> Loss of height
    >> Kyphosis
  • Pathological fractures
    >> Femoral neck fracture
    >> Distal radius (Colles) fracture
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4
Q

What are the possible treatments for osteoporosis?

A

>> GO-TO regimen: bisphosphonate +/- SERM

  • Bisphosphonates (e.g. risendronate, etidronate, alendronate etc.)
  • PTH (e.g. teriparatide) - not to exceed 2 years, and must take bisphosphonate after stopping PTH to maintain BMD
  • SERM (e.g. raloxifene)
  • Testosterone/conjugated estrogen replacement
  • Calcitonin spray - Denosumab
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5
Q

What are the side effects of bisphosphonates?

A
  • Errosive esophagitis: needs to remain upright 30 minutes after drug intake
  • Osteonecrosis of the jaw
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6
Q

What are the indications for bisphosphonates?

A
  • Osteoporosis
  • Paget’s disease of the bone
  • Humoral hypercalcemia of malignancy
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7
Q

What are the possible complications of osteopetrosis?

A
  • Pathological fractures
  • Narrowed foramina
    >> Cranial nerve impingement
    >> Cranial nerve palsies
  • Marrow infiltration
    >> Pancytopenia
    >> Extramedullary hematopoiesis
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8
Q

What are some presenting features of Paget disease of bone?

A
  • Increasing HAT SIZE – hats getting too tight
  • Narrowing of the auditory foramen: hearing loss
  • Bone pain and deformities
  • Long bone chalk-stick fractures >> Increased risk for osteosarcoma
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9
Q

What are the stages of Paget disease of bone?

A
  1. Lytic: increased osteoclastic activity
  2. Mixed: increased both osteoclastic/osteoblastic activity
  3. Sclerotic: increased osteoblastic activity
  4. Quiescent: minimal osteoclastic/osteoblastic activity
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10
Q

What is the treatment for Paget disease of bone?

A

Bisphosphonates: alendronate, risendronate etc.

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11
Q

What are the underlying etiologies of osteitis fibrosa cystica?

A
  1. Hyperparathyroidism
  2. Primary pseudohypoparathyroidism (Albright hereditary osteodystrophy)

>> PTH increased >> increased bone turnover with increased osteoclastic activity

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12
Q

What is the defining histological feature of osteitis fibrosa cystica?

A

“Brown tumours” in bone: cystic spaces lined by osteoclasts filled with fibrous stroma and blood

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13
Q

What are the features of McCune-Albright Syndrome?

A
  • Cafe au lait spots
  • Early/Precocious Puberty
  • Abnormal Bone: polyostotic fibrous dysplasia (bone is replaced by collagen and fibroblasts with irregular bony trabeculae)
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14
Q

What is the most common type of hip dislocation? What is the most common cause of the above type?

A

Posterior dislocation of the hip
- Motor vehicle accident: when the knee is flexed and hips slightly abducted –> knee hits the dashboard

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15
Q

What structures can be damaged in a posterior dislocation of the hip?

A
  • Medial circumflex femoral artery
  • Lateral circumflex femoral artery
  • Femoral vein
  • Femoral nerve
  • Head of femur
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16
Q

What is the most common cause of the unhappy triad?

A

Common contact sports injury
- Lateral force applied to a planted leg

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17
Q

What is the unhappy triad?

A
  • MCL
  • ACL
  • Medial or lateral lemniscus
    >> Lateral lemniscus in 56%
    >> Medial lemniscus in 44%
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18
Q

Which cell type do chondrocytes originate from? Which cells do they share this origin?

A

Mesenchymal stem cells

  • Osteoblasts
  • Adipocytes
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19
Q

What is the leading cause of knee pain in patients under age 45?

A

Patellofemoral syndrome

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20
Q

What is the treatment for patellofemoral syndrome?

A
  • Strengthening the quadriceps
  • Stretching exercises
    >> Hamstrings
    >> Calves
    >> Hip
    >> Iliotibial band
  • Minimize activities that put excessive stress on the knee: squatting, kneeling, jogging, stop and go sports
  • Maximize walking and other low-impact exercise
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21
Q

What are the two types of bursitis that can occur at the knee?

A
  • Prepatellar bursitis: housemaid’s knee
  • Infrapatellar bursitis: clergyman’s knee
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22
Q

What are the ligaments most commonly affected in an ankle sprain?

A
  • Anterior talofibular ligament
  • Calcaneofibular ligament
  • Posterior talofibular ligament
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23
Q

What is the management for ankle sprain?

A

RICE

  • Rest
  • Ice: 20 minutes every 2 hours for the first 48 hours
  • Compression
  • Elevation
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24
Q

How does plantar fasciitis present?

A
  • Pain beneath calcaneus: “Heel pain”
  • Pain in the medial arch
  • Pain worse with first steps in the morning and after weight-bearing
  • Local point tenderness at the medial tubercle of the calcaneus
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25
Q

What is the treatment for plantar fasciitis?

A

Medications

  • NSAIDs
  • Local steroid injection

Physiotherapy

  • Dorsiflexion with night splints
  • Stretching of the plantar fascia and Achilles tendon
  • OTC heel inserts

Surgery
- Surgical release of the plantar fascia in severe cases

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26
Q

What are the muscles of the rotator cuff? How does one test their power?

A

SItS
- Supraspinatus
>> Initial 15 degree abduction of the arm
>> Test: empty beer can test
- Infraspinatus and teres minor
>> External rotation
>> Test: external rotation against resistance
- Subscapularis
>> Internal rotation
>> Test: lift-off test

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27
Q

How does one test for shoulder impingement syndrome?

A
  • Jobe’s test (Empty beer can test) – right-most
  • Hawkin’s test – middle
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28
Q

What is the difference between shoulder separation and shoulder dislocation?

A

Shoulder separation: separation of the clavicle from the acromion and the coracoid process

Shoulder dislocation: separation of the humeral head from the glenoid cavity

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29
Q

What structures can be damaged in an anterior shoulder dislocation? MUST KNOW!

A
  • Axillary nerve: test by testing deltoid cutaneous senses
  • Posterior circumflex humeral artery
  • Supraspinatus tendon
  • Bankart lesion >> Anterior glenohumeral ligament and glenoid labrum separation from the articular surface of the anterior glenoid neck
  • Hill-Sachs lesion >> Posterolateral humeral head defect due to abrasion against the anterior rim of the glenoid
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30
Q

What are the two types of epicondylitis?

A

Lateral epicondylitis

  • “Tennis elbow”
  • Tears in wrist extensor tendons

Medial epicondylitis

  • “Golfer’s elbow”
  • Tears in wrist flexor tendons
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31
Q

What is Dupuytren contracture? What is the cause?

A

Contracture of one or more fingers (usually the ring finger) due to painless thickening and contracture of the tendons of the flexors of the palm

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32
Q

What are the risk factors for Dupuytren contracture?

A
  • Family history
  • Age > 40 years
  • Male
  • Alcoholism
  • Smoker
  • Diabetes Mellitus
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33
Q

What is the treatment for Dupuytren contracture?

A

Definitive treatment
- Surgical release

Other forms of treatment

  • Radiation
  • Bacterial collagenase injection
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34
Q

What is adhesive capsulitis?

A

Severe shoulder adhesions that lock the shoulder in place, seen with disuse of the shoulder due to pain or prolonged immobilization

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35
Q

What is the treatment for adhesive capsulitis?

A

Physiotherapy

  • Heat
  • Analgesia
  • Physical therapy to increase range of motion

Medications

  • Glenohumeral joint injection
  • Subacromial joint injection

Surgery
- Break adhesions under anesthesia (painful!)

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36
Q

Name the carpal bones of the hand.

A

So Long to Pinky, Here Comes The Thumb!

Proximal row (Lateral to Medial)

  • Scaphoid
  • Lunate
  • Triquetrum
  • Pisiform

Distal row (Medial to Lateral)

  • Hamate
  • Capitate
  • Trapezoid
  • Trapezium
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37
Q

What condition must one suspect when there is anatomical snuffbox tenderness?

A

Scaphoid fracture (even if X-ray doesn’t show it)

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38
Q

What are the side effects of NSAIDs?

A
  • Gastric ulcers
  • Acute renal failure from renal ischemia
  • Acute interstitial nephritis
  • Fluid retention
  • Aplastic anemia
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39
Q

What are the side effects of aspirin?

A
  • Gastric ulcers and GI bleeding
  • Acute renal failure
  • Tinnitus
  • Hyperventilation
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40
Q

What bon disorder results from excess PTH?

A

Osteitis Fibrosa Cystica

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41
Q

What are the diagnostic criteria for systemic lupus syndrome?

A

Any 4 of the following 11 (MD SOAP BRAIN):

M: Malar rash
D: Discoid rash
S: Serositis - pleuritis, pericarditis
O: Oral ulcers (PAINLESS!)
A: Arthritis (non-erosive, non-destructive, at least involving 2 joints)
P: Photosensitivty
B: Blood - hemolytic anemia, leukocytopenia, lymphocytopenia, thrombocytopenia
R: Renal - lupus (nephritic – diffuse proliferative glomerulonephritis; nephrotic – membranous glomerulonephritis)
A: ANA (anti-nuclear antibody) positive
I: Immunological markers - anti-dsDNA Ab, anti-Smith Ab, anti-phospholipid Abs
N: Neurlogical symptoms - seizures, psychosis

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42
Q

What are the common causes of death in patients with systemic lupus erythematosus?

A
  • Cardiovascular disease
  • Renal disease
  • Infections
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43
Q

List the immunological markers for SLE and their value in diagnosis and disease management.

A

ANA: sensitive, very non-specific

Anti-dsDNA antibody: specific, poor prognosis (esp. for renal disease)

Anti-Smith antibody: specific, no known prognostic value

Anti-histone antibody: suggests drug-induced lupus

Anticardiolipin antibody: causes hypercoagulable state

C3, C4 levels: decreased –> leads to immunosuppression

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44
Q

What are the drugs that can cause drug-induced lupus erythematosus?

A

SHIPP

  • Sulfonamides
  • Hydralazine
  • Isoniazid
  • Phenytoin
  • Procainamide
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45
Q

What are the possible causes for a positive ANA result?

A
  • SLE
  • Rheumatoid arthritis
  • Juvenile idiopathic arthritis
  • Polymyositis
  • Dermatomyositis
  • Scleroderma
  • Mixed connective tissue disease
  • Sjogren’s syndrome
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46
Q

What is the main underlying pathophysiology of scleroderma?

A

Diffuse systemic progressive sclerosis

  • Skin tightening with no wrinkles
  • Digital pitting
  • Distal ulcerations
  • Characteristic facies: mask-like face, tight lips, beak nose and radial perioral furrows
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47
Q

What are the possible systemic manifestations of scleroderma?

A

Gastrointestinal

  • Dysphagia
  • Loss of LES function: GERD, ulcerations and strictures
  • Small bowel hypomotility: diarrhea, bloating, cramps, malabsorption, weight loss
  • Large bowel hypomotility: wide mouth diverticuli on barium study (pathognomonic)

Renal

  • Hypertension
  • “Scleroderma renal crisis”: malignant arterial hypertension, oliguria and microangiopathic hemolytic anemia

Pulmonary

  • Interstitial fibrosis
  • Pulmonary hypertension
  • Pleurisy
  • Pleural effusions

Cardiac

  • Left ventricular dysfunction
  • Pericarditis
  • Pericardial effusion
  • Arrhythmias

Musculoskeletal

  • Polyarthralgias
  • Resorption of distal tufts
  • Low grade myopathy

Endocrine
- Hypothyroidism

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48
Q

What are the two types of scleroderma and what are their characteristics?

A

Diffuse scleroderma

  • Rapid progression
  • Early systemic involvement
  • Widespread skin involvement
  • Anti-DNA topoisomerase I/Anti-Scl 70 antibody

Localized scleroderma (CREST syndrome)
- Limited skin involvement confined to fingers and face
- C: calcinosis
R: Raynaud’s phenomenon
E: Esophageal dysmotility
S: Sclerodactyly
T: Telangiectasia
- More benign clinical course
- Anti-centromere antibody

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49
Q

What is the classical presentation of Sjogren’s syndrome?

A

Can’t see, can’t spit, can’t climb up shit. (Note: Sicca symptoms)

  • Dry eyes: xerophthalmia
    >> Dryness
    >> Conjuncitivits
    >> A feeling of sand in eyes
  • Dry mouth: xerostomia
    >> Dysphagia
    >> Difficulty in swallowing
  • Arthritis

+ Bilateral enlarged parotid glands
+ Dental caries (due to dry mouth)
+ Increased risk for MALT lymphomas

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50
Q

List two complications of Sjogren’s syndrome.

A
  • Dental caries
  • MALT (mucosa-associated lymphoid tissue) lymphoma
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51
Q

What are the immunological markers for Sjogren’s syndrome?

A
  • Anti-Ro (anti-SS-A) antibody
  • Anti-La (anti-SS-B) antibody
  • Rheumatoid factor
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52
Q

What are the “sicca symptoms”?

A
  • Dry mouth
  • Dry eyes
  • Nasal dryness
  • Vaginal dryness
  • Chronic bronchitis
  • Reflux esophagitis

Those with sicca symptoms do NOT necessarily have Sjogren’s syndrome.

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53
Q

What is the mode of inheritance of Duchenne muscular dystrophy?

A

X-linked

>> Frameshift mutation

54
Q

Which protein is affected in Duchenne muscular dystrophy?

A

Dystrophin protein truncation from DMD gene mutation

  • Dystrophin gene DMD has the longest coding region of any human gene
  • Dystrophin helps anchor muscle fibres
  • Loss of dystrophin results in myonecrosis >> accelerated muscle breakdown
55
Q

What is the classical clinical presentation of Duchenne muscular dystrophy?

A
  • Muscle weakness beginning in the pelvic girdle muscles and moving superiorly
  • Pseudohypertrophy of calf muscles
    >> Calf muscles replaced by fibrous fatty tissues
  • Gower maneuvre
    >> Patient rolls from supine to prone
    >> Uses hands to walk him/herself up
    >> Hands placed on the knees for support
    >> Pushes back upright
  • Waddling gait

>> Onset before 5 years of age

56
Q

What is the most common cause of death in Duchenne muscular dystrophy?

A

Dilated cardiomyopathy

57
Q

What are some investigations to confirm the diagnosis of Duchenne muscular dystrophy?

A
  • CDK: elevated
  • Aldolase: elevated
  • Western blot for truncated DMD protein
  • Muscle biopsy to visualize muscle fibres and for further investigations
58
Q

What is the normal function of dystrophin?

A

Helps anchor muscle fibres in skeletal and cardiac muscles

59
Q

What is the difference between the genetic causes of Duchenne and Becker muscular dystrophy?

A
  • Duchenne: X-linked frameshift mutation
  • Becker: X-linked point mutation
    >> Less severe than Duchenne
    >> Onset in adolescence or early adulthood
60
Q

What is fibromyalgia?

A

Excess muscle tenderness in 11 of 18 particular spots

  • Low cervical
  • Second rib
  • Lateral epicondyle
  • Knee
  • Occiput
  • Trapezius
  • Supraspinatus
  • Gluteus
  • Greater trochanter

>> Benign course

61
Q

What is the presentation of a patient with fibromyalgia?

A
  • Excess muscle tenderness in at least 11 of 18 particular tender points
  • Chronic generalized pain
  • Fatigue
  • Sleep disturbances
  • Headache
  • Cognitive difficulty
  • Mood disturbances

>> 30% have depression and/or anxiety

62
Q

What is the treatment for fibromyalgia?

A

Pharmacological treatment

  • Pregabalin: anticonvulsant
  • Milnacipran: SNRI
  • Amitriptylline: TCA
  • Fluoxetine: SSRI
  • Low-dose analgesics: NSAIDS, acetaminophen

Non-pharmacological treatment

  • Reassurance
  • Exercise and stretching
  • Sleep optimization
  • Relaxation techniques
  • Stress reduction
63
Q

Anti-Smith Abs and Anti-dsDNA Abs

A

Systemic lupus erythematosus (SLE)

64
Q

Anti-histone antibodies

A

Drug-induced lupus

SHIPP:
Sulfonamides
Hydralazine
Isoniazid
Procainamide
Phenytoin

65
Q

Anti-centromere antibodies

A

CREST (localized) scleroderma

Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia

66
Q

Anti-Ro antibodies and Anti-La antibodies

A

Sjogren’s syndrome

Anti-Ro = Anti-SSA
Anti La = Anti-SSB

67
Q

Anti-Jo-1 antibodies

A

Polymyositis

Elevated aldolase
Elevated CPK/CK
Positive ANA

68
Q

Anti-DNA topoisomerase 1 antibody

A

Diffuse systemic scleroderma

69
Q

What are the layers of the epidermis?

A

Californians Like Girls in String Bikinis.

  • Stratum corneum
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale

>> No blood vessels in the epidermis
>> All vasculature in the dermis

70
Q

Name the epithelial cell junction.

  • Cadherins
  • Connects to actin
  • Loss of E-cadherin promotes metastasis
A

Zonula adherins/Intermediate junction

>> Cadherins: Calcium-dependent adhesion proteins

71
Q

Name the epithelial cell junction.

  • Claudins
  • Occludins
A

Tight junctions/Zonula occludens

72
Q

Name the epithelial cell junction.

  • Intermediate filaments
  • Keratin
  • Desmoplakin
  • Pemphigus vulgaris
A

Macula adherens/Desmosomes

>> Pemphigus vulgaris: anti-desmosome or anti-desmoglein antibodies

73
Q

Name the epithelial cell junction.

  • Connexons
A

Gap junctions

>> Cardiac myocytes

74
Q

Name the epithelial cell junction.

  • Integrins
  • Bullous pemphigoid
A

Hemidesmosomes

75
Q

What do fibroblasts produce?

A
  • Collagen
  • Glycosaminoglycans
  • Glycoproteins
  • Reticular fibres
  • Elastic fibres
76
Q

Where do melanocytes originate from?

A

Neural crest cells

77
Q

Where do melanocytes reside in?

A

Stratum basale

78
Q

What is another name for verrucae?

A

WARTS

79
Q

What is another name for warts?

A

Verrucae

80
Q

What are the pathological features of warts/verrucae?

A
  • Epidermal hyperplasia
  • Hyperkeratosis
  • Koilocytes (warts are due to HPV infection)
81
Q

What do you call a wart/verruca in the genital area?

A

Condyloma acuminatum

82
Q

What is another name for the common mole?

A

Melanocytic naevus

83
Q

What is another name for a melanocytic nevus?

A

The Common Mole

84
Q

What is another name for freckles?

A

Ephelis

85
Q

What is another name for ephilis?

A

Freckles

86
Q

Which type of hypersenstivity causes allergic contact dermatitis?

A

Type IV (delayed type) hypersenstivity

  • Nickel
  • Poison ivy
  • Poison oak
  • Neomycin
87
Q

What are the four things that create acne?

A
  1. Hyperkeratosis
  2. Sebum overproduction
  3. Propiobacterium acnes proliferation
  4. Inflammation
88
Q

What is the treatment for acne?

A

Hyperkeratosis

  • Vitamin A analogs
  • Retinoids (e.g. tretinoin, isotretinoin)

Sebum overproduction

  • Isotretinoin
  • Spironolactone
  • Estrogen (OCPs)

Propiobacterium acnes proliferation

  • Erythromycin
  • Tetracycline/doxycycline
  • Topical clindamycin
  • Benzoyl peroxide

Inflammation
- Short term/injectable steroids
>> Remember that long-term steroids will induce acne – Cushing’s!

89
Q

What is the treatment for psoriasis?

A

Topical treatment

  • Emollients and moisturizers
  • Steroids
  • Tar-containing creams
  • Vitamin D analogs
  • Retoinoids
  • Phototherapy

Systemic treatment

  • Methotrexate
  • Cyclosporin
  • Retinoids
90
Q

What are the changes in the epidermal layers in psoriasis?

A
  • Increased stratum spinosum layer
  • Decreased stratum granulosm layer
91
Q

What are some histological findings specific to or suggestive of psoriasis?

A

Overproduction of skin cells

  • Parakeratosis: nuclei remaining in the stratum corneum layer
  • Increased stratum spinosum layer
  • Decreased stratum granulosm layer
92
Q

What are some clinical features suggestive of or specific to psoriasis? Name 3.

A
  • Plaques and papules with silvery scaling
  • Auspitz sign: bleeding spots from broken scales/plaques/papules
  • Pitting of the nails (similar to a golf ball)

>> 1/3rd of patients with psoriasis will have psoriatic arthritis, which is a type of seronegative spondyloarthropathy that is associated with asymmetric and patchy involvement mainly in the fingers (DIP joints – VS. no DIP joint involvement in RA), spine and sacroiliac joints. Psoriatic arthritis is also associated with dactylitis and the “pencil in cup” deformity on X-ray.

93
Q

What are the clinical characteristics of seborrheic keratosis?

A
  • Flat
  • Greasy
  • Pigmented
  • Tortoise-shell like
  • Horn cysts
  • Looks “stuck-on

>> Common benign neoplasm of older people
>> Also known as senile warts

94
Q

What is the histological characteristics of seborrheic keratosis?

A

Squamous epithelial proliferation with keratin-filled cysts

95
Q

What is the Leser-Trelat sign?

A

Sudden appearance of multiple seborrheic keratotic lesions, indicating an underlying malignancy (e.g. GI, lymphoid malignancies)

96
Q

What is the underlying pathophysiology of albinism?

A

A defect/deficiency in tyrosinase

>> Normal number of melanocytes
>> Decreased melanin production

97
Q

What is the underlying pathophysiology of vitiligo?

A

Autoimmune destruction of melanocytes

>> Irregular areas of complete depigmentation with sharp borders
>> A zone with pigmentation only around the follicles (destruction of the perifollicular melanocytes are relatively spared until later) in the transition zone between normal pigmentation and complete depigmentation

98
Q

What is melasma?

A

Hyperpigmentation associated with:

  • Pregnancy
  • OCP use
  • Hormone replacement therapy
99
Q

Name the lesion.

  • Very superficial
  • Honey-coloured crusting
  • Highly contagious
A

Impetigo

>> Staphylococcus aureus
>> Streptococcus pyogenes
>> Lips and nose, especially in children

100
Q

Name the lesion.

  • Dermis infection
  • Acute
  • Painful
A

Cellulitis

>> Staphylococcus aureus
>> Streptococcus pyogenes

101
Q

Name the lesion.

  • Deep tissue injury
  • Rapidly spreading
  • Extremely tender, even beyond the area of obvious inflammation
  • Crepitus upon palpation
A

Necrotizing fasciitis

  • Streptococcus pyogenes
  • Anaerobic bacteria (Clostridium perfringes, Vibrio vulnificus)
102
Q

Name the lesion.

  • White, painless plaques on the tongue
  • Cannot be scraped off
  • Associated with EBV infection
  • Commonly seen in immunosuppressed individuals (e.g. HIV-positive patients)
A

Oral hairy leukoplakia

103
Q

What is the treatment for necrotizing fasciitis?

A

Urgent aggressive surgical debridement with parenteral antibiotics

104
Q

What is the underlying cause of staphylococcal scalded skin syndrome?

A

Epidermolytic exotoxin A and B of staphylococcus bacteria destroying keratinocyte attachments in the stratum granulosum layer

105
Q

What are the presenting features of staphylococcal scalded skin syndrome (SSSS)?

A
  • Fever
  • Generalized erythematous rash
  • Sloughing of the upper layers of the epidermis
  • Heals completely

>> Commonly seen in infants and children

106
Q

What is the underlying pathophysiology of pemphigus vulgaris?

A

Anti-desmosome or anti-desmoglein antibody (IgG)

>> Autoimmune destruction of the desmosomes

107
Q

What are the classical features of pemphigus vulgaris?

A

DAMN is a vulgar word.

  • Desmosomes
  • Acantholysis
  • Mouth lesions
  • Nikolsky’s sign positive

>> Flaccid intraepidermal bullae caused by acantholysis with involvement of the oral mucosa
>> Nikolsky’s sign: separation of epidermis upon manual stroking of the skin

108
Q

What is the gold standard for diagnosis of pemphigus vulgaris?

A

Punch biopsy of the skin for direct immunofluorescence: reticular/net-like pattern around epidermal cells

109
Q

What is the underlying pathophysiology of bullous pemphigoid?

A

IgG antibodies against hemidesmosomes

>> B for Bullous. B for Basement. B for Bottom.

110
Q

What are the classical features of bullous pemphigoid?

A
  • Less severe than pemphigus vulgaris
  • Tense blisters containing eosinophils
  • Negative Nikolsky’s sign
  • No involvement of the mouth
111
Q

What is the gold standard for diagnosis of bullous pemphigoid?

A

Punch biopsy of the skin for direct immunofluoresence, which shows linear pattern at the epidermal-dermal junction

Bu_ll_ous pemphigoid for _l_inear pattern on I.F.

112
Q

Name the disease.

  • Pruritic lesion
  • Celiac disease
A

Dermatitis Herpetiformis

113
Q

Name the lesion.

A

Erythema multiforme

  • Associated with:
    >> Drugs
    >> Infections
    >> Cancers
    >> Autoimmune disease
  • Target-like lesions with multiple rings and dusky centre showing epithelial disruption
114
Q

What drugs can cause Stevens-Johnson Syndrome?

A
  • Anticonvulsants
    >> Carbamazepine
    >> Phenytoin
    >> Ethosuximide
    >> Lamotrigine
    >> Phenobarbital
  • Sulfa drugs
  • Penicillins
  • Allopurinol
115
Q

What are the classical features of SJS?

A
  • Fever
  • Bulla formation and necrosis
  • Sloughing of the skin
  • Rash similar to erythema multiforme
  • Involvement of at least 2 mucous membranes
116
Q

What is the difference between Stevens-Johnson Syndrome and toxic epidermal necrolysis?

A

Toxic epidermal necrolysis (TEN): when SJS involves more than 30% of the body surface area

117
Q

What conditions is acanthosis nigricans associated with? Name 2.

A
  • Hyperinsulinemia
  • Underlying visceral malignancy
118
Q

Which epidermal layer is affected in acanthosis nigricans?

A

Stratum spinosum

(Hyperplasia of stratum spinosum)

119
Q

Name the lesion.

  • Premalignant to squamous cell carcinoma of the skin
  • Sand-paper like on palpation
  • Treat with 5-fluorouracil (5-FU)
A

Actinic keratosis

120
Q

What is erythema nodsum?

A

Painful inflammatory lesions of subcutaneous fat, usually on the anterior shins

121
Q

What conditions are associated with erythema nodosum?

A
  • Crohn’s disease
  • Sarcoidosis
  • Coccidioidomycoses, histoplasmosis
  • Tuberculosis, leprosy
  • Group A streptococcus infection
122
Q

Describe the appearance lichen planus.

A
  • *The 6 Ps of Lichen Planus**
  • Pruritic
  • Purple
  • Polygonal
  • Planar
  • Plaques
  • Papules

+ Wickham striae (reticular white lines)
+ Sawtooth infiltrate of WBCs in histology at the dermal-epidermal junction

123
Q

What disease is lichen planus related to?

A

Hepatitis C

124
Q

Name the lesion.

  • Herald patches, usually on the trunk and back
  • Christmas tree distribution of rash
  • Self-limiting within 6-8 weeks
  • Helped by sunlight exposure
A

Pityriasis rosea

125
Q

Name the lesion.

  • Rolled edge with central ulceration
  • Pearly nodules
  • Telangiectasia
  • Palisading nuclei
A

Basal cell carcinoma

126
Q

Name the lesion.

  • Keratin pearls
  • Actinic keratosis
A

Squamous cell carcinoma

>> Keratoacanthoma: a variant that grows rapidly within 4-6 weeks and may regress spontaneously over months
>> Locally invasive
>> Rarely metastasizes

127
Q

Name the lesion

  • S-100 tumour marker
  • Depth correlates to risk of metastasis
A

Melanoma

128
Q

How does one identify a melanoma?

A

_ABCDE _for melanoma

A: Asymmetry
B: Border irregularity
C: Colour variation
D: Diameter >6mm
E: Evolution over time

129
Q

What is the most common skin cancer?

A

Basal cell carcinoma

130
Q

What are the common locations for tophi in a patient with gout?

A
  • External ear
  • Olecranon bursa (elbow)
  • Achilles tendon
131
Q

What amino acids are commonly found in large concentrations in collagen?

A
  • Glycine
  • Proline
  • Hydroxyproline
    + Lysine
    + Hydroxylysine
132
Q

What are the steps to collagen synthesis?

A
  1. Synthesis of collagen alpha chains (preprocollagen)
  2. Hydroxylation
    >> Requires vitamin C
    >> Proline and lysine residues
  3. Glycosylation
    >> Procollagen: triple helix of 3 alpha-collagen chains
    >> Glycosylation of hydroxylysine residues
    >> Osteogenesis imperfecta
  4. Exocytosis
  1. Proteolytic processing
    >> Cleavage of disulfide-rich terminal regions
    >> Tropocollagen (insoluble)
  2. Cross-linking
    >> Covalent lysine-hydroxylysine cross-linkage
    >> Cu2+-containing lysyl oxidase
    >> Ehlers-Danlos syndrome