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Pathophysiology > Class #12 > Flashcards

Class #12 Flashcards

1
Q

What does “Tinea” mean?

A

refers to a fungal infection

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2
Q

What is the formal name for ringworm?

A

Tinea Corpus

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3
Q

How is tine corpus transmitted?

A

puppies
kittens
other children

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4
Q

How might my patient with tinea corpus present to me?

A
  • circular/oval lesions on trunk, back, buttocks
  • red papule with sharp borders, central clearing
  • puritis, mild burning, erythema
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5
Q

What fungal infection presents with red circular or oval lesions with a central clearing?

A

tinea corpus (ringworm)

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6
Q

What is tine capitis?

A

a fungal infection that manifests on the top of the head, usually in children

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7
Q

What is the difference between primary tinea capitis and inflammatory tines capitis?

A

Primary: gray, found hairless patches
Inflammatory: delayed hypersensitivity with pustular, scaly round patches. This can evolve to a bacterial infection

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8
Q

What is the formal name for athletes foot?

A

tinea pedis

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9
Q

Why might I suspect my patient has athletes foot?

A

inflamed, blistery lesions between toes and on the soles and sides of feet, with a specific foul odour

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10
Q

Who is most at risk for acquiring tinea pedis?

A
  • men
  • barefoot in swimming pools and saunas
  • sharing socks with someone with the infection
  • recurrence with exercise/sweating
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11
Q

A common yeast-like fungus is called…

A

Candidiasis, by candida albicans. Commonly found in GI tract, mouth and vagina, and other warm moist areas of the skin

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12
Q

What causes oral candidiasis?

A
  • long term antibiotic use/oral corticosteroids

- early sign of HIV

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13
Q

How will my patient with candidiasis present?

A

red rash with well-defined borders.

  • puritis, burning
  • can form pustules, which indicates infection
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14
Q

What is impetigo?

A

a bacterial infection (caused by staphylococci or streptococci)
-manifests as small vesicle on the face that ruptures honey-coloured serous drainage that hardens and crusts over

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15
Q

What bacteria causes cellulitis?

A

normal skin flora that become opportunistic OR exogenous bacteria

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16
Q

What is cellulitis?

A

deeper bacterial infection of the dermis and subcutaneous tissue

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17
Q

How is cellulitis transmitted?

A

handling fish
swimming
animal bites

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18
Q

In morning report, I am informed that my patient has cellulitis on her lower legs bilaterally. How will I expect her to present?

A
  • red, warm, edematous, shiny skin
  • may be flaky
  • pain
  • possible fever
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19
Q

What is my concern if my patient with cellulitis is not treated properly?

A

septicemia

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20
Q

What is necrotizing fasciitis?

A

rare bacterial infection usually caused by streptococcal bacteria that involves DEEP skin and facial plan of subcutaneous tissue

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21
Q

What puts an individual at risk for acquiring necrotizing fasciitis?

A
  • immunocompromised
  • cancer
  • diabetes
  • recent major infection
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22
Q

How will my patient with necrotizing fasciitis present?

A
  • red, swollen, painful area that expands quickly!
  • signs and symptoms of inflammation/infection
  • progresses to sepsis
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23
Q

How is necrotizing fasciitis treated?

A
  • QUICKLY
  • high doses of antibiotics
  • surgical debridement
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24
Q

What are verrucae?

A

small tray-white flat papules with rough surface, Warts caused by benign HPV lesions

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25
Q

How are verrucae transmitted?

A
  • direct contact via break in the skin

- sexual contact for genital warts

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26
Q

What does herpes simplex virus cause? How does it manifest?

A

cold sores

-burning, tingling pustules on face, mouth and nasal septum that crust and heal

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27
Q

How is herpes simplex transmitted?

A
  • direct contact with infected saliva

- skin contact via athletics, dentistry and health care

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28
Q

Explain the pathophysiology of shingles

A
  • occurs as a result of reactivation of latent varicella zoster virus infection
  • virus lays dormant in dorsal root ganglia, travels up dermatome and becomes active
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29
Q

Who is at risk for acquiring shingles?

A

-history of chicken pox (varicella zoster)
-old age
-HIV or immunosuppression
-malignancies
-corticosteroid/chemo/
radiation therapy

30
Q

What are the manifestations of herpes zoster?

A
  • burning pain
  • pruritis
  • sensitive skin
  • vesicles form on skin surface, erupt, crust, and fall off. It usually lasts around 2-6 weeks
31
Q

What are the possible complications of herpes zoster?

A
  • neuralgia 1-3 months after skin clears

- Blindness if contact with eyes

32
Q

What are 2 main differences between herpes simplex and herpes zoster?

A
  1. simplex lasts 1-2 weeks whereas zoster lasts zoster lasts 2-6 weeks
  2. simplex is contagious to anyone via saliva or direct contact with the open sore, whereas zoster is only contagious to those who have not had chicken pox, and those individuals will only acquire chicken pox, not shingles.
    3 . simplex is self-limiting with no real complications, whereas zoster can result in severe nerve pain, and even blindness
33
Q

This skin disorder is caused by increased testosterone in puberty

A

acne vulgaris

34
Q

What is the difference between inflammatory and non-inflammatory acne vulgaris?

A

non-inflammatory AV: is caused by sebaceous glands becoming plugged. Blackheads are caused by melanin, and whiteheads indicate fatty acid irritation
Inflammatory: pustules, nodules, cysts

35
Q

What is rosacea? How does it present?

A

a chronic inflammatory skin disorder that causes repeated blushing episodes in the nose and cheesks that eventually remains permanently

  • inflammatory facial pustules, nodules, edema
  • dry, itchy eyes
  • telangiectasia
  • skin thickens and is sensitive to heat
36
Q

What is psoriasis? How does it manifest?

A

autoimmune skin inflammation that occurs in the 3rd decade.
- well defined red plaques with silver scales that are flat or raised on the elbows, knees, scalp, lumbosacral/intragluteal cleft

37
Q

Who is at risk for acquiring psoriasis?

A
  • heredity

- age (30s)

38
Q

What is a complication of long-term psoriasis?

A

hyperkeratosis, which is epidermal thickening overtime, which causes permanent damage to capillaries, and leads to bleeding points under the scales

39
Q

What is the difference between UVA and UVB rays?

A

UVA- not absorbed by ozone, cause deep penetration that causes a tan immediately
UVB-most absorbed by ozone, causes a delayed response that is more genotoxic (burn)

40
Q

Why does a sunburn increase the risk for skin cancer?

A

-burns cause free-radical formation and damage to cellular proteins and DNA

41
Q

Explain the pathophysiology of how UV radiation causes a sunburn

A

UV radiation hits melanocytes

  • some UV reaches lower skin layers
  • immune cells and DNA are damaged
  • inflammatory mediators are released
  • sunburn
42
Q

How does a first degree burn manifest?

A
  • only outer epidermis
  • pink, red, dry, painful
  • skin can still function
  • 3-10 days
43
Q

How deep in the skin does a second degree burn penetrate?

A

epidermis and dermis

44
Q

Explain the difference between a partial thickness second degree burn and a full thickness second degree burn

A 
PARTIAL
-moist blisters that weep
-sensitive to touch, heat, air
-intact blisters help maintain body fluids
-1-2 weeks to heal
FULL
-epidermis and into DEEP dermis
-mottled pink, red or waxy skin with flat, dry blisters, edema
-loss of sensation
scarring
-hair follicles and sweat glands remain intact
- 1 month to heal
45
Q

How deep is a third degree burn?

A

subcutaneous tissue, muscle and bone

46
Q

What are the manifestations of a 3rd degree burn?

A
  • waxy white, yellow, or tan/brown/black
  • EDEMA
  • no pain in areas with 3rd degree, but they experience 1st and 2nd degree pain
47
Q

How is the “rule of nines” different for kids then for adults?

A
  • in adults, the head is 9%, in kids its 18%

- in adults, each leg is 18%, in kids, they are 13.5%

48
Q

What does the “rule of nines” refer to?

A

a reference for measuring what percentage of the body has been affected by the burn

49
Q

What are the hemodynamic complications of burns?

A
  • injury to capillaries and surrounding tissues

- fluid loss leads to hypovolemic shock

50
Q

How can smoke inhalation damage the respiratory system?

A
  • carbon monoxide, toxins, ammonia, chlorine, sulphur dioxide poisoning
  • damaged mucosa can cause bronchospasm, edema
  • pneumonia, pulmonary embolism, pneumothorax
51
Q

Explain the hypermetabolic response to 3rd degree burns

A
  • catecholamine and cortisol released in response to stress
  • muscle/fat wasting, glucose stores depleted
  • head production is increased d/t heat losses from burned area
52
Q

When a burn encircles the whole body or an entire body part, what is is called?

A

circumferential

53
Q

What is the healing process for a circumferential burn?

A

healing to eschar becomes leathery, and constricts, so it must be removed by either escharotomy or fasciotomy

54
Q

List some ways to treat burns

A
  • active cooling
  • fluids
  • hemodynamic balance
  • nutrition
  • analgesia
  • wound care
55
Q

What are the 4 types of grafts used to treat burns?

A
  1. Autograft- from own body
  2. Homograft-from another person (dead or alive)
  3. Heterograft (from another species)
  4. Synthetic
56
Q

Explain why shearing force can cause decubitus ulcers

A

shearing is when the skeleton moves but the skin doesn’t. This causes cell injury and thrombosis from the inside out

57
Q

What are the 4 causes of decubitus ulcers?

A
  1. Pressure
  2. Shearing
  3. Friction
  4. Moisture
58
Q

Why does moisture on the skin increase the risk for the development of ulcers?

A

weakens the cell wall by changing the pH of the skin

59
Q

How does friction cause ulcers?

A

damages dermis/epidermis interface

60
Q

Why does pressure increase the risk for ulcers?

A

obstructs blood flow causing ischemia to the skin

61
Q

What type of nevi have the capacity to develop into a malignant melanoma?

A

dysplastic nevi, which present as rough, irregularly shaped moles with a pebbly surface

62
Q

Who is most at risk for developing malignant melanoma?

A
  • increased UV light exposure
  • h/o blistering sunburns
  • family history
  • h/o dysplastic nevus syndrome
  • fair hair, skin and freckles
  • immunosuppression
63
Q

Explain what malignant melanoma looks like

A
  • mole that is slightly raised, with an irregular border and surface
  • independent from previous nevi
  • often mottled
  • may have erythema, tenderness, ulceration, bleeding
64
Q

Explain the 2 ways that malignant melanoma can grow

A 
RADIAL
-horizontal spread in the epidermis
VERTICAL
-invades deeper dermis
-raised dome lesion
-increased risk of metastasis
65
Q

Your patient was just diagnosed with basal cell carcinoma. How can you explain this to her?

A
  • neoplasm of the basal layer of the epidermis
  • most common neoplasm
  • RARELY metastasizes
  • SLOW-GROWING
66
Q

Describe nodular basal cell carcinoma

A

small, flesh coloured, or pink translucent nodule enlarging overtime

67
Q

Describe superficial basal cell carcinoma

A

scaly erythematous patch/plaque on the surface of the skin

68
Q

What is squamous cell carcinoma?

A

malignant tumor on sun exposed area that is confined to the epidermis for a long time and then converts to invasive stage usually in the older population

69
Q

What are the risk factors to acquiring squamous cell carcinoma?

A
  • UV exposure
  • Arsenic, industrial tar, coal, paraffin
  • Men, but rare if of African descent
70
Q

What does squamous cell carcinoma look like?

A

red-scaling, slightly elevated with irregular border

  • can contain shallow chronic ulcer with crust
  • can metastasize if not excised early
71
Q

What are the ABC’s for diagnosing malignant melanoma?

A 
Assymmetry
Border irregularity
Color variation
Diameter > 6mm
Evolution

Pathophysiology (10 decks)

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