MSK-Skin-CT Flashcards
1
Q
4 lab tests used in SLE (Lupus) Detection?
A
- Antinuclear antibodies ANA present (sensitive, but not specific for SLE)
- Antibodies to dsDNA (very specific, poor prognosis)
- Anti-Smith antibodies (anti-Sm)-very specific, but not prognostic
- Antihistone antibodies (more sensitive for drug induced lupus)
2
Q
Consequences of NEPHRITIS vs NEPHROTIS in SLE Lupus?
A
Nephritic——>profilerative glomerulonephritis
Nephrotic—–>membranous glomerulonephritis
3
Q
Mnemonic for SLE Lupus?
What does each letter stand for?
A
I'M DAMN SHARP!! I=Immunoglobins/antibodies (anti-dsDNA, anti-SM, anti-phospholipid) M= Malar Rash D= Discoid Rash A= ANA= antinuclear antibody M=mucositis (oropharyngeal ulcers) N= neurologic disorders S=serositis (pleuritis, pericarditis) H= hematologic disorders A=Arthritis R= Renal Disorders P=Photosensitivity
4
Q
Target Demographics for SLE Lupus?
A
- 90% = women
- black women mostly
- aged between 14 and 45 usually
5
Q
Other SLE Lupus associated symptoms not included in the mnemonic
A
- False positives on syphillis tests (RPR/VDRL)
- Presentation often includes weight loss and any of the symptoms in the mnemonic
- Libman-Sacks endocarditis (verrucous, wart-like, sterile vegetations on both sides of the valve.)
- Hilar adenopathy
- Raynaud’s phenomenon
6
Q
Conditions associated with sarcoidosis?
Name 6
A
- Restrictive Lung Disease
- Uveitis
- Erythema Nodosum
- Bell’s Palsy
- Hypercalcemia
- Epithelial granulomas containing microscopic Schaumann and asteroid bodies
7
Q
Lab findings on Polymyositis/Dermatomyositis?
Name 3 things
A
- Increased Creatinine Kinase(CK)
- positive antinuclear antibodies (ANA)
- positive anti-Jo-1 antibodies
8
Q
Characteristics/ Clinical Symptoms of Dermatomyositis?
Name 5, including the three rashes
A
- heliotropic rash
- malar rash
- Gottron’s papules on knuckles, elbows, knees
- shawl and face rash
- mechanic’s hands
- increased risk of occult mailgnancy
9
Q
Differences between polymyositis and dermatomyositis?
A
polymyositis= inflammation of the endomysium with CD8+ cells
dermatomyositis= inflammation of the perimysium and atrophy with CD4+ cells
MNEMONIC: muscle is deeper (endomysium), needs cytotoxic T-cells!!
10
Q
Two types of scleroderma and the antibodies associated with each of them?
A
- DIFFUSE: widespread skin involvement, early visceral involvement, and rapid progression…
Antibody= Scl-70, which is anti-DNA topoisomerase - CREST SYNDROME: much more benign of the two with minimal skin involvement limted to fingers and face.
Antibody= ant-Centromere antibody
11
Q
Mnemonic for the benign form of Scleroderma?
A
CREST SYNDROME= more benign than Diffuse scleroderma
CREST: C=Calcinosis R=Raynaud's Phenomenon E=Esophageal dysmotility S=Sclerodactyly T=Telengiectasia
12
Q
Primary Defect in Albinism?
A
decrease in melanin production due to decreased activity of tyrosinase
13
Q
What is hyperpigmentation associated with pregnancy or OCP use called?
A
Melasma (aka chloasma)
14
Q
What are the involved symptoms in the triad of atopic dermatitis?
A
- Allergic Rhinitis
- Asthma
- Eczema (Atopic Dermatitis)
15
Q
Primary defect in Vitiligo?
A
decrease in NUMBER of melanocytes
16
Q
Typical Causes of Erythema Multiforme?
A
Infections: Mycoplasma Pneumonia and HSV
Drugs: B-Lactams, sulfa drugs, Phenytoin
Cancers
Autoimmune Disorders
17
Q
The 6 P’s of Lichen Planus?
A
- disease occurs at the epidermal/dermal junction leading to influx of lymphocytes that form a classical SAWTOOTH appearance at the junction.
- usually associated with Hepatitis C
- Pruritic
- Purple
- Planar
- Polygonal
- Papules
- Plaques
18
Q
Primary defect in Ephelis (freckle)?
A
Increased melanin pigment, but normal number of melanocytes
19
Q
Which diseases/agents are associated with the following skin conditions?
- Verucca (warts)
- Dermatitis Herpetiformis
- Bullous Impetigo
- Erythema Multiforme
A
Verucca (warts): HPV
Dermatitis Herpetiformis: Celiac Disease
Bullous Impetigo: S. Aureaus and S.Pyogenes
Erythema Multiforme: Infections(mycopasma neumoniae, HSV), drugs, cancers, autoimmune disorders
20
Q
Which diseases/agents are associated with the following skin conditions?
- Acanthosis Nigricans
- Erythema Nodosum
- Lihen Planus
A
Acanthosis Nigricans: Hyperinsulinemia (DM, obesity, Cushings Syndrome) and Visceral Malignancy
Erythema Nodosum: Sarcoidosis, Coccidiodoycosis, histoplasmosis, TB, streptococcal infections, leprosy, Crohn’s
Lihen Planus: Hepatitis C
21
Q
Which diseases/agents are associated with the following skin conditions?
- Cellulitis
- Necrotizing Fasciitis
- SSSS
- Hairy Leukoplakia
A
Cellulitis: S. Pyogenes or S.Aureus
Necrotizing Fasciitis: anaerobic bacteria or S.Pyogenes
SSSS: S.Aureus
Hairy Leukoplakia: EBV (usually in HIV patients)
22
Q
Treatment for unresectable metastatic melanoma?
What is the primary genetic defect?
A
Rx= Vemurafenib, a BRAF kinase inhibitor.
Defect is in: BRAF V600E mutation
NB: BRAF is a kinase downstream of RAS.
23
Q
What do intradermal melanocytic nevi look like?
A
Papular
24
Q
What do junctional melanocytic nevi look like?
A
Flat Macules.
25
What do you call a wart on genitalia, that is caused by HPV?
Condyloma acuminata
26
What is Leser Trelat Sign?
Sudden appearance of multiple seborrheic keratoses. This indicates an underlying malignancy---usually GI or Lymphoma
27
Xeroderma Pigmentosum
Defect in enzymes that are necessary for nucleotide-excision repair pathway in removing thymidine dimers. Thus, this defect leads to increase in risk for Squamous Cell Carcinoma
28
Premalignant lesions for Squamous Cell Carcinoma?
1. Actinic Keratoses
| 2. Keratoacanthoma...well-differentiated SCC that develops rapidly and also regresses rapidly.
29
Premalignant lesions for Melanoma?
Melanocytic Nevi (There are two types: junctional which are flat and intradermal, which are nodular)
30
What are the 4 different subtypes of Melanoma? Where is the lesion in skin layers and what is the prognosis for each?
1. Superficial Spreading Melanoma= good prognosis because melanocytes are only growing in the epidermis and epidermal junction [Radial Growth]
2. Nodular Melanoma= bad progonosis because the malignant meanocytes are now growing deep into the dermis. [Vertical Growth]
3. Lentigo Maligna Melanoma= good prognosis because the melanocytes are only growing along the epidermal-dermal junction (Radial Growth)
4. Acrolentiginous Melanoma= affects palms and soles only. Not caused/related to UVB radiation and mostly affects darker skinned people e.g. blacks and Asians
31
Dermatology-related fact about Bob Marley?
Death was caused by acrolentiginous melanoma which was present under his toe nail
32
What are the risk factors for Cellulitis?
Recent Surgery
Trauma
Insect Bite
***often starts with a skin break resulting from the above.
Just like Impetigo, it's caused by S.Aureus or S.Pyogenes, BUT cellulitis affects the deeper dermis, whereas impetigo is only limited to superfcial structures
33
Which virus causes Kaposi Sarcoma?
HHV8- human herpes virus type 8
34
What type of hypersensitivity is allergic contact dermatitis?
What type of hypersensitivity is atopic dermatitis (eczema)?
Contact Dermatitis: Type IV
Eczema: Type I
35
What type of hypersensitivity is Urticaria?
What type of hypersensitivity is Erythema Multiforme?
U: Type I
EM: Type IV
36
Features of Staph Scalded Skin Syndrome? Name 4 classic ones.
1. usually happens in neonates, babies, children or adults who are immunocompromised or in renal failure.
2. caused by exotoxin of staphylococcal which attacks keratinocytes in granulosum
3. results in widespread peeling and sloughing of upper epidermis layers,fever, erythematous rash
4. heals spontaeously
37
Classic Histologic findings in Seborreic Keratoses
| Name 2
PSEUDO-HORN CYSTS (keratin-filled cysts) on flat, greasy, pigmented squamous epithelial proliferation: EPITHELIAL HYPERPLASIA
38
Classic Histologic findings in Basal Cell Carcinoma?
| Name 1
Palisading Nuclei
39
Classic Histologic findings in Verruca Vulgaris?
| name 3
1. Koilocytic features. A koilocyte is a cell that has undergone a number of changes
2. Epidermal Hyerplasia
3 Hyperkeratosis
40
Classic Histologic findings in SLE?
| Name 1
Granular complement an IgG at the dermal-epidermal junction
41
Where is the site of latency for the following viruses?
```
HSV1
HSV2
VZV
EBV
CMV
```
HSV1: Trigeminal ganglia
HSV2: sacral ganglia
VZV: dorsal root ganglia
EBV: B-cells
CMV: Macrophages
42
Which bone condition can result from primary hyperparathyroidism?
Osteitis Fibrosa Cystica
| --expansile cystic masses "brown tumor" in bone, which can be easily confused for bone neoplasm
43
Primary defect in senile osteoPOROSIS (Type II)?
Aging-related loss of osteoblastic activity
44
Primary defect in postmenopausal osteoPOROSIS (Type I)?
Increased osteoclastic activity caused by the relative absence of estrogen
45
Primary defect in Osteomalacia/Rickets?
Poor bone mineralization...usually, Vit D is required in the uptake of Calcium
* *hallmark is widened osteoid bone due to hyperactivity of osteoblasts and poor mineralization
* *nonetheless, bone remains soft and weak
46
Primary defect in Paget's Disease (osteitis deformans)?
Excessive osteoclast activity followed by exuberant, but structurally unsound-osteoblast deposition of bone
47
Primary defect in Achodroplasia (dwarfism)?
point mutation in the FGFR3 gene, which leads to constitutive activation of FGFR3.
When hyperactive, it inhibits chondrocyte proliferation...normal epiphyseal growth plate expansion is suppressed.
AUTOSOMAL DOMINANT
48
Primary defect in OsteoPETROSIS?
Reduced osteoclast activity, defective bone remodeling and hence, "stone bone" that fractures easily.
49
Primary defect in Osteigenesis Imperfecta (OI)?
Defective sythesis of Collagen type I (which forms the extracellular matrix of bone and other parts of the body e.g. eye )
Type I OI is fatal and Type I patients have normal life span and may have blue scelrae, hearing loss, and misshapen teeth
50
Primary defect in Osteoarthritis (OA))?
Degeneration of articular cartilage [degenerative]
essentially =chondrocyte loss not able to keep up with the damage
**Bone changes etc are all secondary changes
51
Histologic Findings in OA?
| Describe the pathologic steps (~7) and histological findings at each of those
1. Decrease in concentration of proteoglycans and increase in water
2 vertical and horizontal fibrilation of cartilage and matrix (as cartilage is degraded)
3. Bone Eburnation: appearance of polished ivory (caused by friction smoothing the surface of now-exposed subchondral bone)
4. Cancellous bone becomes sclerotic and thickened
5 Fracture gaps allow synovial fluid to sip into the subchondral space---->forms subchondral cysts
6. Osteophytes develop at the end of the articular surface
7. EXTERNALLY, Heberden nodes in the fingers are prominent: they represent prominent osteophytes at the DIP joints
52
Where the two different types of nodes in OA?
Heberden nodes in DIP~~~~~ (HD TV)
Bouchard nodes in PIP~~~~~ (BP cuff)
**There is no MC involvement in OA
53
What are the 4 main seronegative spondyloarthropathies? Describe the main feature of each and their main target areas
These are arthritic diseases , without the Rheumatoid Factor (IgM that binds to IgG).
1. Psoriatic Arthritis (joint pain and stiffness):
- pencil in cup joint deformity on X-ray
- sausage fingers (Dactylitis)
- asymmetric and patchy involvement
- less than 1/3 of psoriatic patients have this
2. Ankylosing Spondylitis (spine and sacroiliac joints):
- Fused vertebrae (bamboo spine)
- Uveitis
- Aortic Regurgitation
3. Inflammatory Bowel Disease (ankylosing s, or periheral arthritis):
- -Crohn's and UC
4. Reiter's Arthritis (Reactive Arthritis):
Triad = Conjuctivitis with anterior uveitis
Arthritis
Urethritis ***Cant climb, can't pee, can't
see****
54
What is Sjogren's syndrome?
What causes it?
What are the classic symptoms? (findings)
DEF: inflammatory disease, in which lymphocytic infiltration targets exocrine glands (esp Salivary and Lacrimal) therefore no tears and no saliva
CAUSE: intolerance to CD4+ cells (disease is immune-mediated)
SYMPTOMS:
Triad: Xeropthalmia (dry eyes, with conjunctivitis)
Xerostomia (dry mouth, with dysphagia)
Arthritis
**Diseased is associated with RA and there is marked increase in risk for
B-cell Lymhoma (NHL)--->Parotid Enlargement
and Dental Caries (tooth decay)
55
What are the hematologic findings in Sjogren's syndrome?
Autoantibodies to ribonucleotide protein (RNP):
- SS-B (La)
- SS-A (Ro)
***We Ro-La-ing in our Sjogren****
56
Most common cost of Gout?
| Less common cause of Gout?
90%: due to renal underexcretion
| 10%: Due to overprodution
57
Which diseases/drugs can lead to Gout? Name at least 5
1. Lesch-Nyhan syndrome(defect in HGPRT)
2. PRPP excess (used in both denovo and salvage purine synthesis)
3. Decreased excretion of uric acid (e.g. due to thiazide diuretics)
4. Increased cell turnover
5. von Gierke's disease
58
Drugs used to treat:
a) Chronic Gout?
b) Acute Gout?
Drugs used to treat Pseudogout?
a) Chronic: Febuxostat, Allopurinol---both are xanthine oxidase inhibitors
b) Acute: glucocorticoids, colchicine, NSAIDs e.g. indomethacin
59
Primary defect in gout?
Primary defect in pseudogout?
Which age groups are affected in either disease?
Gout: precipitation of monosodium urate (uric acid) crystals out of blood into joint space
-common in men
Pseudogout: Deposition of calcium pyrophosphate (CPP) crystals within the joint space.
- usually caused by defect in enzymes that degrade or make the calcium crystals
- common in people over 50yo. Men and Women equally affected
60
Crystal appearance of Gout vs. Psedogout?
Gout: Negatively birefringent. Appear yellow under parallel light
Pseudogout: Negatively birefringent. Appear blue under parallel light
61
Dfferential Diagnosis for Gout?
| Name 3
- Lesch-Nyhan Syndrome (Xs uric acid production due defect in HGPRT enzyme)
- G6Pase deficiency (von Gierke's disease--glycogen storage disease)--gout due to increased muscle breakdown as glycogen cannot be broken down
- Alcoholism (because alcohol metabolites compete for the same excretion sites in kidney as uric acid)
62
Causes of avascular necrosis AVN ...aka Osteonecrosis
Infarction of bone and marrow due to:
1. Trauma
2. Corticosteroid Use (Fat embolism because corticosteroids can deposit in the marrow leading to Xs fat)
3. Sickle Cell anaemic (oclusion of vessels due to aggregation--->cyanosis---->ischemia)
4. Alcoholism (messes up fat metabolism in the liver and then::::fat emboli again!)
63
Typical Features of Gonococcal arthritis?
| Other causative agents of infectious arthritis?
Gononococcus arthritis = S.T.D.
S= synovitis (e..g. knee)
T= tenosynovitis (e.g. hand)
D= dermatitis (e.g. pustules)
Other causative agents are: S. Aureus, Streptocossus, N.Gonorrhoeae, Salmonella (for people with Sickle-Cell Disease)
64
1) What causes Duchenne's Muscular Dystrophy
2) Features of Duchenne's Muscular Dystrophy?
Name 4
3) Difference between DMD and BMD
X-linked frame-shift mutation of the dystrophin gene.
Patients have almost zero dystrophin on immunohistochemistry
1) accelrated muscle breakdown
2) weakness begins in pelvis and then clims up the shoulders and other proximal structures
3) Pseudohypertrophy of claf muscles
4) Patients use Gower's maneuver
5) Onset is usually before 5yo and patients are usually dead by 20yo
in BMD, its an X-linked mutation and symptoms are less severe and more variable than DMD
--onset is usually during adolescents and patinets almost have a normal lifespan
65
Features of Fibromyalgia?
Name 5
Which patient population is usually targeted?
Women in the range 20-50yo
Features:
-chronic musculoskeletal pain
asssociated with: ---stiffness
---paresthesia
----poor sleep
----fatigue
***NO WEAKNESS (just like polymyalgia rheumatica)
66
Primary Defect in Myasthenia Gravis?
Primary Defect in Lambert-Eaton myasthenic syndrome?
MG: autoantibodies against post-synaptic Acetyl-choline receptors
LE: autoantibodies against presyaptic calcium-voltage-gated channels.
67
Disorder(s) associated with Myasthenia Gravis?
Disorder(s) associated with Lambert-Eaton myasthenic syndrome?
MG: -thymic hyperplasia
-thymoma
LE: -small cell lung cancer. Lambert Eaton is usually a para-neoplastic outcome, but it may occur without the thymic hyperplasia
68
Features of Myasthenia Gravis?
Name 3
Treatment of MG?
features: -ptosis
- diploplia
- muscle weakness
Rx: AChE inhibitor
thymic resection
plasmapharesis
prednisone
69
Primary cause of Myositis Ossificans
Trauma
70
Differentiation origin of osteoblasts?
Secretion products of Osteoblasts?
Origim: Mesenchymal stem cells in periosteum
Products: Secrete Collagen and catalyze mineralization
71
Differentiation origin of osteoclasts?
Secretion products of Osteoclasts?
Origin: monocytes/macrophages
Products: acid and collagenases
72
Main difference between a wrist Median N lesion (laceration or carpal tunnel) and a proximal injury (supracondylar fracture)?
Proximal: Pope's Benediction results
Wrist Damage: Median Claw (just the lumbricals affected, but the lateral 2 flexor digitorum profundii and the superficiali are still intact)
73
Nerve root innervation of the rotator cuff muscles?
Actions of each of the rotator cuff muscles?
Roots: C5 and C6
Supraspinatus: ABDucts the first 10-15 degrees, before deltoid kicks in.***most commonly damaged***
Infraspinatus: laterally rotates arm. ***pitching injury***
teres minor: laterally rotates and ADDucts arm
Subscapularis: medially rotates and ADDucts arm
74
Which muscle(s) protects the brachial plexus from injury?
SUbclavius Muscle
75
Findings in Erb-Duchenne Palsy?
| Name 3
a.k.a as "WAITERS TIP"..usually due to upper trunk damage during delivery. Damage is to C5 and C6 roots
Findings:
1) Limb is held close to body (paralysis of abductors)
2) Medial Rotation (due to paralysis of lateral rotators)
3) Forearm is pronated (loss of biceps)
76
Common causes of Klumpke's Palsy?
| -Name 3
Klumpke's palsy is damage to inferior trunk: C8 and T1 roots.
Usually caused by
1) embryonic or chidbirth defect affectig the inferior trunk
2) cervical rib compressing trunk
3) pancoast tumor
If a cervical rib compresses both the subclavian artery and the inferior trunk---then=THORACIC OUTLET SYNDROME
77
Common source of damage to long thoracic nerve?
Outcomes of damage? Name 2
Source of damage: mastectomy
Outcomes: 1) winged scapula
2) ipsilateral lymphedema
78
3 major anatomic landmarks?
xxx
79
Mode of inheritance of Achondroplasia?
A. dominant
80
Mode of inheritance of O. Imperfecta?
A. dominant
81
Treatment for osteoPETROSIS?
Bone Marrow Transplant because the pimary defect is in the osteoclasts: osteoclasts are essentially macrophages and macrropahges are derived from moncytes...and monocytes come from hematopoeisis in the Bone Marrow!
82
Prophylaxis for Osteoporosis?
- exercise of weiught-bearing joints
- Vit D supplements
- Calcium supplements
83
In osteomyelitis, where does the bacteremia seed in children versus in adults?
children: metaphysis
adults: epiphysis
84
From which germ layer does Ewing's sarcoma arise from?
NEUROECTODERM!!
85
Diseases that have malar rash as a characteristic?
- Dermatomyositis
| - SLE (lupus)
86
Joint Findings in RA?
| **Name 5***
Pannus formation in joints (MCP and PIP)
Subcutaneous Rheumatoid Nodules (fibrinoid necrosis)
Ulnar deviation of fingers (boutonnierre deformities)
Subluxation
Baker's cysts in Popliteal fossa
87
receptors in skeletal muscle fibers in a NMJ junction?
nicotinic
88
Which 3 disease modifying agents are often used in the treatment of RA?
- Methotrexate
- Sulfasalazine
- TNF-a inhibitors
89
Which drugs are often implicated in drug-induced lupus?
- procainamide
- hydralazine
- INH
- Phenytoin
