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Musculoskeletal System > Integumentary DLA > Flashcards

Integumentary DLA Flashcards

1
Q

What is hyperkeratosis?

A

Thickening of the stratum corneum

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2
Q

What is parakeratosis?

A

Retention of nuclei in the keratinocytes of the stratum Corneum

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3
Q

What is acanthosis?

A

Increase in thickness of the stratum spinosum

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4
Q

What is acanthylosis?

A

Broken bonds between cells of the epidermis leading to separation of these cells from each other

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5
Q

Describe basal cell carcinoma

A
  • UV light
  • proliferation of basal stem cells
  • Dark nuclei with sparse poorly defined cytoplasm
  • Cells at the periphery has a characteristic palisades appearance
  • Central cells are more randomly arranged
  • Invades the dermis and deeper lying structures
  • Does not typically metastasize
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6
Q

What are the predisposing factors of squamous cell carcinoma?

A
  • sunlight (UV)
  • industrial carcinogens
  • chronic ulcers
  • tobacco chewing
  • burns
  • ionizing radiation
  • betel nut chewing
  • arsenic exposure
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7
Q

What is most common location of squamous cell carcinoma?

A

More common in head and neck region (likely due to excessive sunlight exposure)

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8
Q

What is squamous cell carcinoma?

A
  • Malignant tumor of keratinocytes
  • exposure to UV with DNA damage (inactivation of P53 gene)
  • loss of elderly in nuclear size and shape
  • Hyperkeratosis and Parakeratosis
  • Common in elderly (above 70 years)
  • fair skinned > dark skinned
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9
Q

Describe the histological evaluation of squamous cell carcinoma

A

Dermis deeply infiltrated by islands and sheets of malignant squamous cells

The islands have undifferentiated cells, resembling basal cells, around the parameter

Islands show squamous differentiation with formation of squamous pearls or swirls

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10
Q

What is malignant melanoma?

A
  • malignant transformation of melanocytes
  • causes highest number of skin cancer related deaths in US
  • more common in whites, Australia/ South Africa
  • etiology- exposure to sunlight (UV) light : types- Acute, intermittent, blistering
  • increased number of melanocytes with large atypical morphology- arranged at the dermo-epidermal junction

May invade the dermis- metastases(fatal)

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11
Q

What is melan A?

A

Immunohistocheemistry marker, a specific antibody that stains malignant melanoma cells

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12
Q

What is albinism?

A

Genetic (autosomal recessive)

  • loss of pigmentation of the skin, hair, and eyes
  • Lack of tyrosinase
  • types: ocular, oculocutaneous
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13
Q

What are the long term implications of albinism?

A
  • skin cancers
  • reduced visual acuity/photophobia (macular hypoplasia)
  • social stigma
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14
Q

What is Vitiligo?

A
  • Depigmentation disorder
  • auto-immune
  • destruction of melanocytes
  • types: focal, segmental, generalized
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15
Q

How can vitiligo be treated?

A

Medical:
-topical steroid therapy

  • Psolaren photochemotherapy
  • Depigmentation

Surgical:
-Autologous skin graft

  • Micropigmentation
  • Melanocytes transplants
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16
Q

What is Psoraisis?

A

A chronic inflammatory and hyper proliferative disorder of the skin

  • Clinically manifested as well-circumscribed, erythema toes and itchy plaques covered with slavery scales( knees, elbows, lower back, scalp)
  • Epidural turnover averages 8-10 days

Characterized by hyperkeratosis and parakeratosis

17
Q

What are the predisposing factors of psoriasis?

A
  • genetic background

- inciting background (stress)

18
Q

Explain the pathogenesis of psoriasis

A
  • Exogenous/endogenous antigens: predisposing factors
  • Antigen presentation by APCs: Langerhans cells
  • T-lymphocyte-mediated immune response
  • Cytokine secretion
  • Inflammation & cellular hyperproliferation
  • Clinical lesions of psoasis
19
Q

What is parakeratosis?

A

Retention of nuclei in the stratum corneum

20
Q

What causes epidermal removal in psoarisis?

A

Parakeratosis

  • prominent itchy areas with increased skin scaling and peeling
  • epidermal hyperplasia- increased rate of proliferation

This leads to shedding of the epidermis constantly, resulting in scales seen as whitish patches

21
Q

What is Bollous pemphigod?

A
  • damage to hemidesmosomes- separation of epidermis & dermis
  • Chronic autoimmune blistering disease: skin & mucous membranes (bulla large fluid filled vesicles)
  • Antibodies (IgG) specific to hemidesmosomes bind to basement membrane and stimulate leukocytic infiltration
  • Eosinophils releases proteases that degrade hemidesmosomes
  • Fluid accumulation-blistering formation
  • Characteristic by large blisters that don’t easily rupture
22
Q

What is Pemphigus vulgaris?

A

Pemphix(blister/bubble)

  • Rare autoimmune disorder affecting epidermis and mucosal epithelium
  • Desmosomes- separation of the stratum spinosum keratinocytes one from another
  • Antibodies target cadherins and desmoplakins and desmogleins
  • Atrophy of the prickle cell layer
  • Blister formation: easy to rupture- Nikolsky’s sign, skin shears off easily
23
Q

What causes ACNE?

A

Inflammation of a sebaceous gland

  • Affects 85-100% of people at some point in life
  • Genetic predisposition
  • Common in adolescents (prior to onset of puberty- adrenal androgens): in all age groups
  • Affects face, back, chest upper arm- areas with increased sebaceous glands
24
Q

What are wound healing?

A

Skin damage in motion a sequence of events that repairs the skin to its normal (or near normal) structure and function

2 types:

  • epidermal wound healing
  • deep wound healing
25
Q

Contrast epidermal and deep wound healing

A

Epidermal wound healing- occurs following wounds that affect only the epidermis

Deep wound healing- occurs following wounds that penetrate the dermis

26
Q

What is epidermal wound healing?

A
  • In response to an injury, the basal cells of the epidermis surrounding the wound, break contact with the basement membrane, enlarge and migrate across the wound
  • The cell migrate from opposite sides until they meet (in a sheet-like formation)
  • Epidermal growth factor stimulates basal stem cells to divide and replace the lost cells, that have moved into wound
  • These new cells divide to thicken the new epithelium
27
Q

What is deep wound healing?

A
  • As the injury involves multiple tissue layers, healing process is more complex. Healing involves scar formation and can include loss of function
  • This type of healing occurs in 4 phases:
  • Inflammatory phase(up to 3 days after wound)
  • Migratory phase
  • Proliferative phase(from the 3rd day to weeks after the wound )( type III collagen dominant)
  • Maturation phase
28
Q

Describe the inflammatory phase of deep wound healing

A

Blood clot is formed and loosely attaches the cut edges. Vasodilation and increased permeability helps neutrophils and monocytes(which become macrophages) to enter the area and eliminate microbes, foreign material and dying tissue.

Mesenchymal cells develop into fibroblasts

29
Q

Describe the migratory phase of deep wound healing

A

As the clot becomes a scab, epithelial cells migrate beneath it to bridge the wound. Fibroblasts synthesize scar tissue (collagen and glycoprotein ) and damaged vessels regrow

This now constitutes the granulation tissue

30
Q

Describe proliferative phase of deep wound healing

A

Growth of the epithelial tissue at random. Continued growth of vessels

31
Q

Describe the maturation phase of the deep wound healing

A

Scab sloughs off. Epidermis restored to normal thickness. Collagen is more organized. Fibroblasts decrease and blood vessels stabilize.

This type of scar- fibrosis

32
Q

Contrast hypertrophy scar and keloid scar

A

Hypertrophic scar- raised more than normal, but within original wound boundary
-Mainly type III collagen in well organized rows

Keloid scar- in excess of the boundary, and extending into surrounding tissue
-Mainly highly disorganized types I and III collagen

  • More common in persons who are darker skinned
  • Common location#- ear, neck, sternum, upper extremities
33
Q

What is the purpose for a rule of nine’s?

A

Used to describe burn coverage over the body(and indirectly severity)

34
Q

What are first degree burns?

A

Partial thickness epidermis only

Heals spontaneously

35
Q

What are secondary degree burns?

A

Partial thickness epidermis and dermis

Epithelial water barrier disrupted

Heals spontaneously

36
Q

What is a third degree burn?

A

Full thickness epidermis, dermis and subcutaneous tissue

Water barrier disrupted , nerves and blood vessels destroyed.

Does not heal spontaneously, fluid loss is extensive

Musculoskeletal System (41 decks)

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