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HD 2 > Ortho + Path (skin & bone) > Flashcards

Ortho + Path (skin & bone) Flashcards

0
Q

Lichenoid reaction (skin)

A

inflammation along dermal-epidermal junction.

  • -> vacuolar change & cell death.
    (4) : Lichen planus, Erythema Multiforme, Lupus, Graft vs. Host
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1
Q

3 factors that affect peak bone mass

A
  1. genetics
  2. physical activity
  3. nutrition
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2
Q

Lichen Planus (skin) pathology

A

Gross: - Koebner phenomena - “P’s” = pruritic, plateaued papules
- Wickham stria (reticular, lacy patterns on mucosal surface),
Histo: compact hyperkeratosis, hypergranulosis, & liquefactive degeneration (w/ colloid bodies)

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3
Q

Erythema Multiforme pathology

A

Gross: target lesions = minor, skin sloughing = severe.
Histo: necrotic keratinocytes, spongiosis, dermal edema, lymphocytic infiltration, (normal basket-weave corneum)

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4
Q

Graft vs. Host skin pathology

A

Gross: erythematous, BLANCHABLE macules (severe = bullae), ~4 wks after transplant.
Histo: necrotic keratinocytes & liquefactive necrosis at basal layer.

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5
Q

Lupus skin pathology

A

Gross: “butterfly rash” on face, w/ spared labial folds.
Histo: follicular plug, liquefactive necrosis w/ lymphocytes @ DEJ (“bubbly, vacuolar basal cells)

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6
Q

Psoriasiform skin reaction

A

epidermal hyperplasia w/ regular, elongated Rete Ridges;

3): Psoriasis, lichen simplex chronicus, pellagra (*collar rash!

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7
Q

Psoriasis pathology

A

Gross: salmon colored plaque w/ silvery scale, Koebner phenom., & Auspitz sign (appears in areas of minor trauma)

Histo: Dilated papillary dermal vessels (Auspitz) & confluent parakeratosis.

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8
Q

Lichen Simplex Chronicus (skin) Pathology

A

= from chronic/excessive rubbing & scratching
Gross: leathery appearance (esp. hands, elbows)
Histo: Jagged Rete Ridges & vertical streaked collagen

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9
Q

Spongiotic skin reaction pattern

A

= intraepidermal intracellular edema,
*chronic => Lichenification
(4): eczema (atopic dermatitis), contact (irritant or allergic) dermatitis, sebhorreic dermatitis
Path: edema fluid btwn keratinocytes –> accentuate desmosomes.

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10
Q

“epidermotropism”

A

refers to directed emigration of lymphocytes into lower epidermis;
= malignant process.
*ie: mycosis fungoides!

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11
Q

Vesiculobullous (skin) reaction pattern

A

= vesicles or bullae (blistering) anywhere in epidermis;

(6): herpes, dermatitis herpetiformis, Scalded skin syndrome, impetigo, bullous pemphigoid, pemphigus vulgaris.

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12
Q

Scalded Skin Syndrome

A

(from staphylococcal exotoxin)
*vesicular fluid = sterile!
Histo: sloughed stratum corneum, rest of epidermis = intact.

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13
Q

Impetigo

A

Gross: honey-colored crust/eschar, (from staph aureus)
* CAN culture bacteria directly from bullous fluid
Histo: Crust & bacteria @ corneum, w/ perivascular lymphocytes.

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14
Q

bullous pemphigoid

A

autoimmune disorder esp. in elderly,
Gross: tense, pruritic blisters
Histo: subepidermal blisters w/ intact acanthocytes.

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15
Q

Pemphigus vulgaris

A

= autoimmune destruction of desmoglein III, @ mucus membranes!
Gross: Nikolsky’s sign (loose blister, shifts w/ pressure)
Histo: intraepidermal splitting, suprabasilar vesicle; w/ Acantholysis & “tombstone” row.

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16
Q

dermatitis herpetiformis

A

cutaneous blistering associated w/ gluten sensitivity (IgE!);
Gross: symmetrical eruptions (esp. hands, forearms)
Histo: subepidermal blister, many Eosinophils & neutrophils!!!
(also: IgA deposited @ tips of dermal papillae)

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17
Q

Leukocytoclastic vasculitis

A

= non-blanching erythema –> purpura;

Histo: vascular & fibrinoid necrosis (of vessel wall), + extravasated RBCs

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18
Q

Acanthosis nigrans pathology

A

= thick, hyperpigmented skin.
80% benign (childhood/puberty/youth onset DM2)
20% malignant (occult adenocarcinoma).
Histo: Basal cell layer hyperpigmentation, + hyperkeratosis

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19
Q

Verruca vulgaris pathology (skin)

A

Rete ridges slope inward!

also: supraepidermal hemorrhage, hyperkeratosis & hypergranulosis…

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22
Q

Dysplastic nevus pathology

A
  • more likely to become malignant (skin neoplasm).
  • melanocyte bridging btwn Rete Ridges
  • melanocyte nesting = poorly organized
23
Q

Spitz nevus pathology

A

LESS concerning skin neoplasm,

  • well-circumscribed
  • no (abnormal) mitotic activity
24
Q

junctional vs. compound vs. intradermal nevus pathology

A

= hyperpigmented macules; = nest of melanocytes…
Junctional: @ DEJ only
Compound: @ DEJ & within dermis
Intradermal: within dermis only

25
Q

Lentigo pathology

A

= skin neoplasm,

increased pigment WITHIN keratinocytes @ DEJ

26
Q

Dermatofibroma pathology

A

Gross: benign, hyperpigmented plaque. + pinch test
Histo: Tabled Rete ridges & whorling spindle cells

27
Q

dermatofibrosarcoma protruberans pathology

A

well-differentiated primary fibrosarcoma, @trauma/scar site;
locally aggressive, does NOT spread to lymph nodes, recurs.
Histo: storiform pattern (whorling spindle cells), spindle cells infiltrate adipose tissue.

28
Q

Mycoides fungoides/Cutaneous T cell Lymphoma pathology

A

Gross: scaly brown plaques/patches w/ diffuse erythema;
Histo: cerebric, lymphocytic epidermotrophism (“Pautrier microabscess”) + perakeratosis.
*“Sezary Syndrome” = in blood

29
Q

Merkel Cell carcinoma pathology

A

(neural crest derived)
Gross: dark, round, nodular
Histo: small, round, blue cells infiltrating dermis

30
Q

Basal Cell Carcinoma pathology

A

Nodular: clustered basal cell proliferation, w/ peripheral palisading edges
Sclerosing: basaloid strands & fibrosis

31
Q

Actinic keratosis pathology

A

Gross: premalignant plaque –> freeze off
Histo: parakeratosis & atypical keratosis w/ lymphocytic infiltration

32
Q

Keratoacanthoma pathology

A

Gross: rapid growing, skin colored nodule w/ keratotic plug
Histo: localized, well-differentiated carcinoma (similar to SCC)

33
Q

Melanoma pathology (general)

A

Histo: pagetoid melanocytes, atypical melanocytes, hemorrhage

34
Q

layers of cartilage & their function

A
  1. Tangential - resist shear forces, high amt collagen type IX & H2O
  2. Transitional - resist compression
  3. Radial - distribute load, vertical organization
  4. calcified - hyaline cartilage, next to bone; CAN scar/heal in this layer only.
35
Q

5 things to check for in emergency setting

A 
ABCDE: 
Airway
Breathing 
Circulation
Disability/deformity
Environment/exposure (ie: infection)
36
Q

Signs of acute compartment syndrome

A

Pain out of proportion to injury & w/ passive stretch, tense mm compartment, paresthesia, paralysis and progression.
Treat with fasciotomy.
(Do NOT Tx w/ fasciotomy IF late (>8hrs) –> irreversible injury, limb = nonfunctional or avascular, or if coagulopathy)

37
Q

True orthopedic emergencies

Fatal if no intervention within minutes - hours

A
  1. Vascular injury
  2. Acute compartment syndrome
  3. Intra capsular hip fracture (–> hemodynamic instability)
  4. Spinal cord injury
  5. Rapidly expanding infection (ie: necrotizing fasciitis)
38
Q

Consequences of missed acute compartment syndrome

A
  1. Ischemic contractures
  2. Renal failure
  3. Amputation
  4. Death
39
Q

Intramembranous bone formation

A

Direct bone formation of flat bones from mesenchymal condensation.
(Only early in dvpt)
–> skull, spine & pelvis

40
Q

Endochondral bone formation

A

Formation of long bones by deposition of osteoid into cartilage framework.

  • occurs at growth plates
  • -> bones of limbs
41
Q

Parts of bone

A

Diaphysis: shaft of bone, = thick, cortical (= lamellar)
Metaphysis: small area of trabecular bone btwn diaphysis & epiphysis
Epiphysis: articular surface (end), separated from metaphysis by growth plate

42
Q

Components of bone extracellular matrix (4)

A
  1. Mineral matrix (esp. hydroxyapetite/Ca)
  2. Organic matrix (type I collagen)
  3. Water
  4. Cells (ostoblasts, osteoclasts, osteocytes)
43
Q

Types of bone cells

A

Osteoblasts: make bone, = mesenchymal
Osteoclasts: break down bone, = multi-nucleated giant cells
Osteocytes: regulate mineral homeostasis

44
Q

Primary bone healing

A

With surgery & hard cast,
=> rigid immobilization and precise approximation,
Osteoblasts deposit bones on cones along fracture

45
Q

Secondary bone healing

A 
Self-healing fracture, 
=> cartilage laid to form scar, then osteoblasts remodel into bone. 
Stages: 
1. Hematoma/inflammation
2. Callus (scar)
3. Remodeling (self-healing)
46
Q

Normal blood flow direction in bone vs abnormal (with fracture)

A

Normal BF: outward from center of bone to edges

W/ fracture: BF toward center of bone (bc change in P)

47
Q

Positive Galeazzi sign

A

In infants to Dx developmental dysplasia of the hip;
w/ baby supine, flex knees so ankles touch butt.
+: knees not even/level
(May have increased, asymmetrical skin crease on leg)

48
Q

Barlow maneuver

A

Tests for developmental hip dysplasia in infant,
Adduct hips w/ light force on knees posteriorly.
+: feel hip dislocate when adducted

49
Q

Ortolani maneuver

A

Test for developmental dysplasia of the hip in infants,
Used with Barlow maneuver, here abduct hips from tucked position (start with knees and hips flexed, legs together)
+: feel hip relocate when abducted (bc dislocated w/adduction)

50
Q

Risk factors for developmental dysplasia of the hip

A
  1. Breech position for birth
  2. Female > male
  3. First born child
  4. Family history of DDH
    * most commonly on left side
51
Q

Major Infectious causes of joint pain in children

A
  • Septic arthritis (bacterial infection of joint, *elevated CRP)
  • toxic synovitis (post-viral hip inflammation; afebrile, normal labs)
  • Lyme infection (joint swelling, test with Lyme titer)
  • osteomyelitis (bacterial infection of bone)
  • juvenile RA (autoimmune, not infectious)*
52
Q

Main findings in osteoarthritis (4)

A
  1. Joint space narrowing
  2. Osteophytes/bone spurs
  3. Sclerosis
  4. Cyst formation
53
Q

Greatest predictor of fracture

A

1: Previous fracture.

*also age: compression fractures VERY common in elderly.

HD 2 (14 decks)

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