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OCHT Term I > Patho - Term Test II (Integumentary System, MSK) > Flashcards

Patho - Term Test II (Integumentary System, MSK) Flashcards

1
Q

Skin accounts for about ___% of body weight.

A

20

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2
Q

Primary function of skin is:

A

Protection (against microorganisms, UV radiation, mechanical stress, and loss of body fluids)

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3
Q

What additional functions does the skin have. Select all that apply.

1) immune surveillance
2) body temp. regulation
3) production of vitamin D
4) Touch and pressure receptors

A

All

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4
Q

The layer that contains macrophages, fibroblasts, fat cells, nerves, fine muscles, blood vessels, lymphatics, and hair follicle roots is known as what?

A

Hypodermis (subcutaneous layer)

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5
Q

Fingernails and toenails are made of what?

A

protective keratinized plates

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6
Q

Describe the fingernail/toenail composition/structure (6).

A

1) proximal nail fold
2) eponychium (cuticle)
3) matrix where the nail grows and its nail root
4) hyponychium (nail bed)
5) nail plate
6) paronychium (lateral nail fold)

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7
Q

What is the approximal rate of nail growth?

A

~1mm or less daily

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8
Q

Hair follicles start from where in the skin?

A

Starts from the matrix/bulb

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9
Q

Hair colour depends on what?

A

melanin-secreting melanocytes in the hair follicle

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10
Q

What do sebaceous glands secrete and what stimulates the growth of these glands?

A

Secretes sebum

Growth stimulated by androgens (so enlargement of these glands = early signs of puberty = oily teenagers)

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11
Q

Sebum is primarily composed of what substance, which allows for what function?

A

Lipids; allows for prevention of hair and skin drying

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12
Q

Sebaceous glands are numermous in which parts on the body?

A

Face, chest, back

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13
Q

Modified sebaceous glands are found where?

A

eyelids, lips, nipples, glans penis, prepuce (foreskin)

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14
Q

The type of gland that is found all over the body (but mostly in palms of hands, soles of feet, and forehead) and involved with thermoregulation is known as?

A

eccrine sweat glands

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15
Q

(Apocrine/eccrine) sweat glands produce more sweat.

A

Apocrine

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16
Q

Where are apocrine sweat glands found?

A

near bulbs of hair follicles in axillae, scalp, face, abdomen, and genital areas

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17
Q

How does perspiration have an odor?

A

Due to interaction of sweat (from apocrine sweat glands) and flora bacteria

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18
Q

Blood supply to skin is supplied by what?

A

papillary capillaries (plexus) of the dermis (and these are supplied by a deeper arterial plexus)

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19
Q

Regulation of body temperature in the skin is faciliated by what vascular structures?

A

Arteriovenous anastomoses (direct connections between small arteries and veins)

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20
Q

How is body temperature/heat loss regulated in the skin? 2 mechanisms.

A

1) variations in skin blood flow through opening and closing of arteriovenous anastomoses
2) evaporative heat loss of sweat

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21
Q

Which nervous symptom regulates vasoconstriction/vasodilation in the skin?

A

SNS - sympathetic nervous system (via alpha-adrenergic receptors in the skin)

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22
Q

Approximately ____ % of heat is lost through the skin.

A

80

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23
Q

Epidermis consists of what 4 types of cells?

A

1) keratinocytes
2) melanocytes
3) Dendritic/Langerhans cells
4) Merkel cells

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24
Q

Layers ot the epidermis (from superficial to deep).

A 
Stratum corneum
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basale
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25
Q

Which of the epidermal cells creates calluses?

A

keratinocytes

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26
Q

Antigen presenting cells involved with immune function of the body are which type of epidermal cell?

A

Langerhans (dendritic) cell

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27
Q

What are Merkel cells and where are they found?

A

aka tactile epithelial cells and are mechanoreceptors for light touch; found in stratum basale

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28
Q

SNS regulates which sweat glands?

A

eccrine (stress and fear activate SNS leading to sweating)

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29
Q

Besides the papillary capillaries, the arterial plexus also supplies blood to where?

A

hair follicles, sweat glands

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30
Q

Marks left on the skin as a result of scratching chicken poxes is an example of what type of lesion?

A

secondary lesion

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31
Q

Define macule and indicate type of lesion

A

Primary lesion; flat, circumscribed area that is a change in the colour of the skin <1cm in diameter

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32
Q

Freckles, flat moles (nevi), petechiae, measles, and scarlet fever are examples of what type of lesion?

A

Macule

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33
Q

Define papule and indicate type of lesion

A

Primary lesion

an elevated, firm, circumscribed area <1cm in diameter

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34
Q

Provide 5 examples of a papule lesion.

A
  • warts (verruca)
  • elevated moles
  • lichen planus
  • fibroma
  • insect bite
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35
Q

Define patch and indicate type of lesion

A

Primary lesion

flat, non-palpable, irregular shaped macule >1cm in diameter

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36
Q

Provide 4 examples of patch lesions.

A
  • vitiligo
  • port wine stains
  • Mongolian spots
  • café au lait spots
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37
Q

Define plaque and indicate type of lesion

A

Primary lesion

elevated, firm and rough lesion with flat top surface, >1 cm in diameter

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38
Q

Psoriasis, seborrheic, and actinic keratosis are examples of what type of lesion?

A

Plaque

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39
Q

Define wheal and indicate type of lesion

A

Primary lesion

elevated irregularly shaped area of cutaneous edema; solid, transient, variable diameter

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40
Q

3 examples of wheal lesions are:

A
  • insect bites
  • hives (urticaria)
  • allergic reaction
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41
Q

Define nodule and indicate type of lesion

A

Primary lesion

elevated, firm, circumscribed lesion that is deeper in the dermis than papule; 1-2cm in diameter

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42
Q

Erythema nodosum and lipomas are examples of what type of lesion?

A

Nodule

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43
Q

Define tumor and indicate type of lesion

A

Primary lesion

elevated, solid lesion that may be clearly demarcated and deeper in dermis (>2cm in diameter)

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44
Q

Neoplasms, benign tumors, lipoma, neurofibroma, and hemangioma are examples of what type of lesion?

A

tumor

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45
Q

Define vesicle and indicate type of lesion

A

Primary lesion

elevated, circumscribed, superficial sac that does not extend into dermis and fill with serous fluid (<1cm in diameter)

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46
Q

Provide 5 examples of vesicle lesions.

A

<1cm in diameter:

  • varicella (chickenpox)
  • herpes zoster (shingles)
  • herpes simplex

> 1cm in diameter:

  • blister
  • pemphigus vulgaris
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47
Q

Define pustule and indicate type of lesion

A

Primary lesion

elevated, superficial lesion that is similar to a vesicle but filled with purulent fluid (milky discharge)

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48
Q

Impetigo and acne are examples of what type of lesion?

A

pustule

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49
Q

Define cyst and indicate type of lesion

A

Primary lesion

elevated, circumscribed encapsulated lesion that could be found in dermis or subcutaneous layer and filled with liquid or semisolid material

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50
Q

Sebaceous cysts and cystic acne are examples of what type of lesion?

A

cyst

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51
Q

Define telangiectasia and indicate type of lesion

A

Primary lesion

fine, irregular lines (0.5-1mm) produced by capillary diffusion (basically dilated superficial blood vessels)

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52
Q

Provide four conditions that are associated with telangiectasia?

A
  • acne rosacea
  • venous hypertension (spider veins in legs)
  • systemic sclerosis
  • developmental abnormalities (port wine birthmarks)
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53
Q

Which level of the skin are fat cells located?

A

Hypodermis (subcutaneous)

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54
Q

Primary lesion vs. secondary lesion

A

Primary: those that develop as a direct reuslt of the disease process

Secondary: those evolve from primary lesions (due to changes in disease progression, patient activities like itching/treatment)

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55
Q

Define scale and indicate type of lesion.

A

Secondary lesion

heaped-up keratinized cells that looks like flaky skin, irregular shaped, may be thick/thin and dry/oily

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56
Q

Provide an example of scale.

A
  • dry skin
  • flaking skin from seborrheic dermatitis (after scarlet fever)
  • flaking skin after drug reaction
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57
Q

Define lichenification and indicate type of lesion.

A

Secondary lesion

rough, thickened epidermis secondary to perisistent rubbing, itching, or skin irritation, and often involves flexor surface of extremity

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58
Q

Provide an example of lichenification.

A

Chronic dermatitis

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59
Q

Define keloid and indicate type of lesion.

A

Secondary lesion

irregularly shaped, elevated, and progrssively enlarging scar that grows beyond wound boundaries

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60
Q

Keloid formations often happen after _____. It is caused by what?

A

Surgery

caused by excessive collagen formation during healing

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61
Q

Define scar and indicate type of lesion.

A

Secondary lesion

Thin to thicken fibrous tissue that replaces normal skin after an injury/laceration to the dermis

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62
Q

2 examples of scars include:

A
  • healed wound

- surgical incision

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63
Q

Define excoriation and indicate type of lesion.

A

Secondary lesion

Loss of epidermis; looks like a linear, hollowed-out crusted area

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64
Q

Provide two examples of conditions that lead to excoriation (excessive itching/picking leading to skin damage) lesions.

A
  • scratches/abrasions (ie scabs)

- scabies

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65
Q

Define fissure and indicate type of lesion

A

Secondary lesion

linear crack or break from epidermis to the dermis; may be moist or dry

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66
Q

Provide any two examples of fissure lesions.

A
  • athlete’s foot
  • cracks at corner of the mouth
  • anal fissure
  • dermatitis
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67
Q

Define erosion and indicate type of lesion.

A

Secondary lesion

loss of part of epidermis resulting in depressed, moist, glistening area (typically follows a rupture of a vesicle/bulla)

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68
Q

Provide an example of erosion lesion.

A

rupture from chemical injury

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69
Q

Define ulcer and indicate type of lesion.

A

Secondary lesion

Loss of epidermis and dermis; concave and variable size

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70
Q

Provide two examples of ulcer lesions.

A

Pressure ulcers

Stasis ulcers

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71
Q

Define atrophy and indicate type of lesion.

A

Secondary lesion

Thinning of skin surface and loss of skin markings; skin becomes translucent and paperlike

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72
Q

Two examples of atrophic lesions include:

A
  • aged skin

- striae (stretch marks)

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73
Q

What are comedones? List its two types.

A

Pores or hair follicles that are plugged with sebaceous and keratin material (oil, bacteria, dead skin cells)

Two types:

  • blackheads (open comedone with dilated opening)
  • whiteheads (closed comedone with narrow opening)
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74
Q

What is a burrow?

A

narrow, raised, irregular channels caused by parasite

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75
Q

What is petechiae?

A

circumscribed area of blood (less than 0.5cm in diameter)

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76
Q

What is purpura?

A

circumscribed area of blood larger than 0.5cm in diameter

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77
Q

Skin damage caused by unrelieved pressure, shearing forces, friction, and/or moisture is known as what?

A

pressure injury

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78
Q

What is the most common cause of a pressure injury?

A

interrupted blood flow to and from skin/underlying tissues

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79
Q

Where do pressure injuries usually develop?

A

over bony prominences (sacrum, heels, ischia, greater trochanters)

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80
Q

How does the skin present when there is temporarily pressure vs. unrelieved pressure?

A

Temp pressure: redness (reactive hyperemia) that eventually goes away, no lasting tissue damage

Unrelieved pressure: platelet aggregation occurs in endothelial cells lining capillaries; blood flow blocked and anoxic necrosis occurs

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81
Q

Shearing/friction forces are mechanical forces moving (parallel/perpendicular) to the skin.

A

parallel (basically dragging someone)

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82
Q

Describe skin presentation in superficial vs deep tissue damage in pressure injuries

A

Superficial damage - layer of dead tissue that forms as an abrasion, blister, erosion (nonblanchable red/darkened skin)

Deeper tissue damage - reddish blue discolouration, closer to the bone

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83
Q

Why is there a foul smell with pressure ulcers?

A

bacteria colonize dead tissue and dissolve it causing foul smell and discharge

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84
Q

Which of the following are risk factors in developing pressure ulcers?

1) prolonged head of bed elevated over 30 degrees
2) neurological disorders
3) vasopressors
4) all of the above

A

4) all of the above

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85
Q

Identify and describe the 4 stages of pressure ulcers.

A

Stage 1: nonblanchable erythema on intact dermis

Stage 2: partial thickness skin loss (in epidermis or dermis)

Stage 3: full thickness skin loss through dermis with visible adipose tissue

Stage 4: full thickness skin loss with exposure of muscle, bone, or supporting structures

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86
Q

Treatment of pressure ulcers include what?

A

priorities: prevention and early detection

  • frequent ax of the skin
  • repositioning
  • promotion of movement
  • implementation of pressure reduction (beds)
  • pressure removal (positioning intervals)
  • pressure distribution devices
  • elimination of excessive moisture and draining
  • debriding necrotic tissue
  • adequate nutrition, oxygenation, fluid balance
  • pain management
  • antibiotics for infection
  • construction of skin flaps for large deep ulcers
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87
Q

How do you treat superficial pressure injury lesions?

A

cover with flat, moisture retaining but not wet dressings that cannot wrinkle or cause increased pressure/friction

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88
Q

Similarities and differences between keloids and hypertrophic scars.

A

Similarities: both caused by abnormal wound healing with excessive fibroblast activity and collagen formation (loss of control of normal tissue repair and regeneration)

Differences:

  • keloids: round firm elevated scars with irregular claw-like margins that extend beyond wound site
  • also appears weeks-months after stable scar is formed
  • hypertrophic scars: elevated erythematous fibrous lesions that stay within injury borders
  • appears 3-4 months after injury and goes back to normal within the year
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89
Q

Common areas at risk for keloid/hypertrophic scars include what? (5 areas)

A
  • shoulders
  • back
  • chin
  • ear
  • lower legs
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90
Q

Who is most likely to develop keloids?

A

dark pigmented skin types

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91
Q

Pruritus is also known as what?

A

itching

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92
Q

Symptoms of pruritus are commonly associated with what? (3 categories)

A

1) primary skin disorders (eczema, psoriasis, insec infestations)
2) systemic disease (ex. chronic renal failure, liver disease, thyroid disorder)
3) use of opiate drugs

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93
Q

True or false. Pruritus can be acute or chronic, localized or generalized, and it can migrate from one location to another.

A

True

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94
Q

An increase in what substance is associated with pruritis?

A

itch mediators????

  • histamine, serotonin, prostaglandins, bradykinins, neuropeptides, acetylcholine, IL-2, IL-31
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95
Q

The two most common inflammtory skin disorders are what?

A

eczema

dermatitis

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96
Q

Eczematous disorders are typically characterized by what?

A
  • pruritus
  • lesions with indistinct borders (erythematous, papules, or scales)
  • epidermal changes
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97
Q

What does chronic eczema skin look like?

A

thick, leathery skin that is hyperpigmented

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98
Q

Continued scratching of skin with eczema/dermatitis will lead to what?

A

edema, serous discharge, and crusting of skin

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99
Q

Allergic contact dermatitis is a common form of ___________ hypersensitivity.

A

T-cell mediated/delayed

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100
Q

What is a common cause of allergic contact dermatitis?

A

poison ivy (Type IV/delyaed hypersensitivity)

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101
Q

Briefly describe the mechanism of allergic contact dermatitis.

A

1) allergin makes contact with skin and binds to carrier protein
2) Langerans cells process antigen and present it to T cells
3) inflammatory cytokines released
4) symptoms of dermatitis

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102
Q

Type IV/delayed hypersensitivity shows up several (minutes/hours/days) after initial contact with allergin.

A

hours

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103
Q

Signs and symptoms of allergic contact dermatitis include what?

A
  • erythema
  • swelling
  • pruritic vesicular lesions where the allergin came in contact with the skin
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104
Q

Treatment of contact dermatitis includes what?

A
  • topical or systemic steroids

- removal of allergen and antigen

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105
Q

Irritant contact dermatitis S/S and treatment resembles what other condition?

A

allergic contact dermatitis

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106
Q

Provide at least two examples of causes of irritant contact dermatitis.

A
  • acids
  • prolonged exposures to soaps and detergents
  • industrial agents
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107
Q

Atopic dermatitis (aka allergic dermatitis) is common in those with a history of what conditions? This condition is common in who?

A

hay fever/asthma

common in infancy and childhood

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108
Q

A patient presents with inflammation and edema in the lower legs, with scaling, petechiae and hyperpigmentation on the skin. This patient also mentioned itchiness and redness on her skin initially. This patient is likely suffering from what skin condition?

A

Stasis dermatitis

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109
Q

What causes stasis dermatitis?

A

Chronic venous stasis, edema (blood pooling in your legs resulting in venous insufficiency) so those with varicose veins, phlebitis, and vascular trauma are susceptible

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110
Q

Treatment for stasis dermatitis includes what?

A
  • elevating legs
  • not wearing tight clothes around legs
  • not standing for long periods
  • antibiotics for infection
  • moist dressings for ulcers, vein ablation surgery
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111
Q

Seborrheic dermatitis is also called what in infants?

A

cradle cap

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112
Q

An excess of which immunoglobulins lead to atopic dermatitis?

A

immunoglobin E (IgE)

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113
Q

The most common cause of eczema in children is what condition?

A

atopic dermatitis aka atopic eczema

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114
Q

Atopic dermatitis presentation on skin is what?

A
  • severe pruritis
  • characteristic of eczema appearance: redness, edema, scaling (dry skin) and easily irritated due to impaired skin barrier function
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115
Q

Rash resulting from atopic dermatitis is common in which areas in children?

A
  • face
  • scalp
  • trunk
  • extensor surfaces of arms and legs
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116
Q

Treatment for atopic dermatitis includes what?

A
  • education
  • avoiding triggers
  • promoting skin hydration (baths, moisturizer)
  • antiinflammatory agents during flare-ups
  • antibiotics, antihistamines for systemic therapy
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117
Q

What is atopic dermatitis?

A

A chronic inflammatory skin condition characterized by dry, itching skin

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118
Q

What are the factors that lead to dermal pressure ulcers?

A
  • Continuous unrelieved pressure
  • friction
  • shearing
  • moisture
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119
Q

What is seborrheic dermatitis?

A

common disorder characterized by chronic inflammation of skin involving scalp, eyebrows, eyelids, ear canals, nasolabial folds, axilla, chest, and back; unknown cause

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120
Q

What are signs and symptoms of seborrheic dermatitis?

A

scaly, white, yellowish inflammatory plaques with mild pruritus

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121
Q

Treatment for seborrheic dermatitis includes what?

A
  • topical therapies (antifungal shampoo, low dose steroids for flare ups, calcineurin inhibitors)
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122
Q

Papulosquamous disorders are conditions characterized by what?

A

Papules, scales, plaques, and erythema

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123
Q

What is psoriasis?

A

A chronic inflammatory and autoimmune disorder that is proliferative and can relapse, and involves the skin, scalp, and nails

papulosquamous disorder

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124
Q

In psoriasis, the skin is _______ (thinned/thickened) due to what? What is the typical appearance of psoriatic skin?

A

thickened; due to excessie proliferation of keratinocytes and endothelial cells (while cell maturation and keratinization is bypassed) leading to plaques, erythema and silvery skin appearance.

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125
Q

What is the most common type of psoriasis? What is the presentation of this type of psoriasis?

A

plaque psoriasis - thick, silvery, scaly, and erythematous plaques surrounded by normal skin ; small papules that can eventually turn into large lesions

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126
Q

A rare type of psoriasis characterized by lesions developing in skin folds (i.e. armpits, groin) is known as _____ psoriasis.

A

Inverse

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127
Q

The condition characterized by small papules presenting on trunk and extremities weeks after a resp. tract infection (strep throat) is known as _________ psoriasis.

A

Guttate

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128
Q

inflammatory arthritis in the hands, feet, knees, and ankle joints of an psoriatic individual is known as what condition?

A

psoriatic arthritis

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129
Q

Pustular psoriasis presents with what lesions on the skin?

A

blisters/red scaly pus-filled bumps (aka pustules)

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130
Q

Psoriasis that results in widespread red, scaling lesions over large body areas is known as __________ psoriasis.

A

erythrodermic/exfoliative psoriasis

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131
Q

What causes pityriasis rosea?

A

herpes-like virus

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132
Q

What is pityriasis rosea?

A

A viral rash that is self-limiting (resolves in a few months) and occurs in trunk, extremities; more often in young adults

papulosquamous disorder

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133
Q

What is the presentation of pityriasis rosea?

A
  • Initial: herald patch (large circular pink spot) usually on the trunk
  • secondary lesions extend to upper parts of extremities
  • looks like a drooping pine tree on the back
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134
Q

Treatment for pityriasis rosea?

A
  • systemic corticosteroids and UV light to control itch

- otherwise self-limiting and will resolve in few months

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135
Q

What is lichen planus?

A

benign autoimmune inflammatory skin and mucous membrane disorder; papulosquamous disorder and self-limiting

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136
Q

The most distressing symptom in lichen planus is what?

A

Pruritus

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137
Q

Signs and symptoms of lichen planus include what?

A

non-scaling, purple, flat, polygonal pruritic papules and lesions appear symmetically on wrists, ankles, lower legs, and/or genitalia

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138
Q

A common consequence of lichen planus lesions is post-inflammatory ________.

A

hyperpigmentation

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139
Q

Treatment for lichen planus includes what?

A
  • topical, intralesional, or systemic corticosteroids

- antihistamines (for itching)

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140
Q

Inflammatory disorder involving the pilosebaceous follicle is known as what? This condition is also known as the typical acne adolescents get.

A

acne vulgaris

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141
Q

In addition to concern about the appearance of their skin, people who have lichen planus are distressed by severe _______.

A

pruritus

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142
Q

The term ____________ can be used interchangeably with the term eczema to describe an inflammatory response in the skin that involves pruritus, lesions with indistinct borders, and epidermal changes.

A

dermatitis

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143
Q

Dermatitis that occurs on the legs as a result of chronic venous stasis is called ____________ dermatitis; dermatitis that involves scaly, yellowish, inflammatory plaques is called ____________ dermatitis.

A

stasis; seborrheic

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144
Q

What is the difference between acne vulgaris and acne rosacea?

A

Acne vulgaris - typical acne common in adolescence

Acne rosacea - chronic, readily exacerbated, inflammatory skin disease that develops primarily in middle age

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145
Q

A severe form of acne resulting in cysts is known as _________.

A

Acne conglobata

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146
Q

Hydradenitis Suppurativa (Inverse acne) is an inflammatory disease involving what glands?

A

deep sections of apocrine sweat glands complicated by fibrosis and draining sinus tracts

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147
Q

Inverse acne is common in apocrine gland-rich areas which include: (4)

A
  • armpit
  • groin
  • perianal region
  • perineum
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148
Q

S/S of inverse acne include what kinds of lesions?

A
  • deep lesions that form painful subcutaneous nodules often with sinus tracts
  • ruptures horizontally under the skin
  • draining fistulas
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149
Q

Treatment of inverse acne includes what?

A
  • topical therapy
  • systemic medication
  • incision and draining nodules
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150
Q

The irreversible bulbous appearance of the nose that occurs in acne rosacea is known as ___________.

A

rhinophyma

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151
Q

What causes acne?

A
  • hormones (androgens)
  • bacteria
  • clogged pores/hair follicles
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152
Q

The following S/S are characteristic of which papulosquamous disorder?

  • flushed, burning sensations
  • sun sensitivity
  • rhinophyma
  • eye disorders
A

acne rosacea

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153
Q

Discoid lupus erythematosus (DLE) is an __________ disease with skin signs and symptoms. It more commonly affects (men/women) in their 30’s-40’s.

A

autoimmune; women

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154
Q

DLE skin lesions are often located where on the skin? How do the skin lesions present in this condition?

A
  • lesions located on light exposed areas of the skin
  • butterfly pattern of distribution over nose/cheeks
  • red plaques with brownish scale that eventually may look like depressed scars
  • may have residual telangiectasia and hypopigmented scarring
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155
Q

Treatment of DLE includes what?

A
  • sun protection
  • use of topical steroids
  • immunosuppressants
  • antimalarial drugs
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156
Q

A common characteristic of vesiculobullous diseases is what type of skin lesion?

A

blister/vesicle formation

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157
Q

What is pemphigus?

A

A group of rare autoimmune blistering diseases of the skin and oral mucous membranes

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158
Q

The most common form of pemphigus is ________. It is caused by what?

A

pemphigus vulgaris

caused by circulating autoantibodies directed against desmosome adhesion molecules in the epidermis resulting in loss of adhesion = fluid accumulation = blister formation

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159
Q

Factors causing pemphigus include are genetic, environmental, and _________ related.

A

endogenous (i.e. emotional/hormonal stressors)

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160
Q

Dx and Tx of pemphigus.

A

Dx: clinical and histological findings (immunofluorescence) of antibodies at site of blister formation

Tx: systemic corticosteroids, and adjuvant immunosuppressants

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161
Q

The vesiculobullous disease characterized by inflammation of the skin and mucous membranes caused by an immunologic reaction to drug/microorganism is known as ________.

A

Erythema multiforme

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162
Q

The most severe form of pemphigus is __________.

A

Paraneoplastic pemphigus

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163
Q

An autoimmune blistering disease known as ____________ has several forms, all of which involve ____________ against proteins involved in adhesion of the epidermis to the dermis.

A

pemphigus; autoantibodies

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164
Q

Lesions in erythema multiforme resemble what shape? what are other S/S of erythema multiforme?

A

Bull’s eye/target

other S/S: urticarial plaques, pruritus, burning

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165
Q

What is the cause of erythema multiforme?

A

immune complexes formed and deposited around dermal blood vessels, basement membranes, and keratinocytes

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166
Q

Stevens-Johnson Syndrome (SJS) vs. Toxic Epidermal Necrolysis (TEN)

A

Both affect skin and mucous membranes and are type IV hypersensitivity to reactions to drugs

but SJS involves 10% of body surface area while TEN involves >30% body surface area

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167
Q

S/S of SJS/TEN include what?

A
  • prodromal symptoms: fever, headache, malsaise, sore throat, and cough
  • bullous lesions that turn into erosions/crusts when ruptured
  • may have difficulty eating, breathing, urinating
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168
Q

Dx and Tx of SJS/TEN include what?

A

Dx: medication hx, skin biopsy

Tx: withdrawal from ongoing drug therapy, treating infection, monitor fluid and electrolyte balance

  • maintain mucous membranes
  • may need wound care from burn unit
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169
Q

Provide 6 examples of bacterial infections leading to skin conditions.

A
  • folliculitis
  • furuncles/carbuncles
  • cellulitis & necrotizing fasciitis
  • erysipelas
  • impetigo
  • lyme disease
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170
Q

Provide 3 examples of viral infections

A
  • herpes simplex virus (HSV)
  • warts
  • herpes zoster and varicella
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171
Q

Provide 2 examples of groups of fungal infections.

A
  • tinea infections

- Candidiasis

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172
Q

A bacterial infection in the hair follicle resulting in pustules and erythema is kown as what condition? It may be caused by prolonged skin _______, skin trauma, _______ clothing, and poor hygiene.

A

Folliculitis; moisture; occlusive

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173
Q

Treatment of folliculitis includes what?

A

Clean with soap and water, topical antibiotics

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174
Q

Furuncles vs carbuncles.

A

Furuncles: boils/abscesses of hair follicles that spreads into surrounding dermis

Carbuncles: collection of furuncles

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175
Q

Carbuncles lead to lesions that present as what?

A
  • firm mass that turns into a erythematous, painful, swollen abscess
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176
Q

Treatment of furuncles/carbuncles includes what?

A
  • warm compress for comfort, promote localization, and spontaneous drainage
  • for severe cases, incisions and draining of abscess and antibiotics
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177
Q

Cellulitis vs. Necrotizing Fasciitis

A

Cellulitis: infection of dermis and subQ tissue by bacteria (can be an extension of other skin wounds like ulcers)

Necrotizing fasciitis: rare, rapidly spreading infection caused by strep. pyrogenes (starts in fascia, muscle, and subQ fat - subsequent necrosis)

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178
Q

Cellulitis Sx and Tx:

A
  • warm, erythematous, swollen, painful
  • usually in lower extremities

Treatment: systemic antibiotics

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179
Q

Treatment for necrotizing fasciitis.

A
  • antibiotics

- surgical debridement to prevent toxic shock syndrome

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180
Q

Erysipelas is described as a bacterial infection affecting what?

A

acute superficial infection of upper dermis

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181
Q

Erysipelas commonly affects which 3 body areas, and what are the S/S?

A
  • face, ears, lower legs

S/S:

  • firm red spots that turn into red hot lesions with raised border
  • possible vesicles
  • pruritus
  • burning
  • tenderness
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182
Q

Treatment of erysipelas includes:

A
  • cold compress

- antibiotics

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183
Q

Impetigo is a (mildly, highly) contagious infection of the skin with streptococci or (gonococci, staphylococci); the lesions begin as (macules, vesicles) that rupture to form a honey-colored (crust, ulcer).

A

highly; staphylococci; vesicles; crust

184
Q

Impetigo is more common in which age demographic?

185
Q

Treatment of impetigo?

A

antibiotics; maintaining good hygiene

186
Q

Impetigo is a contagious bacterial disease occurring in two forms: bullous and vesicular. Describe the cause for each.

A

Bullous impetigo: infection caused by Staphylococcus aureus

vesicular impetigo: infection caused by group A b-hemolytic streptococcus (strep pyogenes) with/without S. aureus

187
Q

Diaper dermatitis (diaper rash) is a form of _______ contact dermatitis. It is caused by what?

A

irritant

  • caused by prolonged exposure to and irritaiton by urine wetness and feces, also from prolonged skin contact to wet diapers/airtight plastic diaper covers
188
Q

Diaper rash can be secondarily infected with what fungus?

A

Candida albicans

189
Q

Diaper rash lesions look like what? Treatment includes what?

A

varied; mild erythema to erythematous papular lesions

Treatment:

  • frequent diaper changes/regular exposure of area to air
  • use super absorbent diapers
  • topical protection and medication
190
Q

Lyme disease is a multisystem inflammatory disease caused by _________ bacteria and is transmitted by ____ bite. It is the most frequently reported _______ illness.

A
  • Borrelia burgdorferi
  • tick
  • vector-borne
191
Q

The 3 stages of lyme disease presentation are:

A

1) localized infection with bull’s eye rash
2) disseminated infection - rash, muscle and joint pain (rare but possible meningitis, neuritis, carditis)
3) late persistent infection - post-lyme disease syndrome

192
Q

treatment of lyme disease?

A

antibiotics

193
Q

HSV-1 vs. HSV-2

A

HSV-1: transmitted via contact with infected saliva leading to infections in the mouth, lips, cornea

HSV-2: transmitted by skin mucous membrane contact during viral shedding - more common in genitals

194
Q

HSV-1 can be provoked and reacted by what factors? (5)

A
  • UV light
  • skin irritaion
  • fever
  • fatigue
  • stress
195
Q

Treatment of HSV?

A

depends on symptoms present; topical or oral antiviral agents

196
Q

Shingles is also known as __________. Chickenpox is also known as _________.

A

Herpes zoster

Varicella

197
Q

What virus causes chickenpox?

A

Varicella-zoster virus (VZV)

198
Q

S/S and Tx of shingles?

A

pain, paresthesia localized to the affected dermatome

Treatment:

  • compresses
  • calamine lotion
  • baking soda
199
Q

Warts are also known as ________. They are benign lesions caused by various _____________.

A

verrucae; human papillomavirus (HPV)

200
Q

Common warts are known as ________ and occur most often in which age demographic and where on the body?

A

verruca vulgaris; children; fingers

201
Q

Wart lesions look like what?

A
  • flat, round, fusiform

- rough elevated grayish surface

202
Q

Treatment for warts includes what?

A
  • cryotherapy
  • electrocautery
  • topical salicyclic acid
  • intralesional agents
203
Q

Venereal warts are also known as _________, are (highly/moderately) contagious and are transmitted how? Treatment includes what?

A

condylomata acuminate; highly; sexually transmitted

Treatment: prophylactic vaccine

204
Q

Dermatophytes cause skin infections which thrive on ________.

205
Q

Fungal disorders are also known as ________. Fungal disorders caused by dermatophyes are known as _______.

A

mycoses; tinea

206
Q

Where does tinea capitis affect on the body, and what causes it?

A

fungal infection of the SCALP; primary microorganism responsible for this disease is Trichophyton tonsurans

207
Q

Lesions and Sx of tinea capitis look like what?

A
  • scaly, pruritic scalp with bald areas

- hair breaks easily

208
Q

Ringworm is also known as ________. Organisms responsible for this disease are _________ and ______.

A

tinea corporis;

organisms:

  • Microsporum canis
  • Trichophyton mentagrophytes
209
Q

Common sources of ringworm? How is it transmitted?

A
  • contact with kittens and puppies

- direct contact with infected lesion or indirect contact with personal items used by someone infected

210
Q

What is Candidiasis?

A

Fungal infection caused by yeast-like fungus (Candida albicans) and normally found on mucous membranes, skin, GI tract, and vagina

211
Q

Where do yeast infections most commonly occur?

A

vagina (i think) - all evidence points to vjayjay

212
Q

What is thrush and what causes it?

A

Fungal infection by C. albicans in mucous membranes of the mouths of infants (keratolytic proteases allow for epidermal barrier to be penetrated through)

213
Q

Cutaneous vasculitis is inflammation of the ____________ and results from what?

A

blood vessel wall

  • results from immune complexes in small blood vessels as a toxic response to drugs, allergens, infection
214
Q

Treatment of cutaneous vasculitis?

A

remove antigen, corticosteroids, immunosuppressants

215
Q

Urticaria is also known as _____. Describe urticarial presentation on the skin.

A

hives; circumscribed area of raised erythema and edema of superficial dermis

216
Q

Treatment of urticaria includes what?

A
  • remove cause of reaction
  • antihistamines
  • corticosteroids/epinephrine
217
Q

What is localized scleroderma (aka morphea)?

A

sclerosis (stiffening) of the skin and underlying tissue

218
Q

What does scleroderma look like? What does it cause?

A
  • shiny patches of hardened or tightened skin/skin streaks

- skin looks taut, hard, hypopigmented

219
Q

Systemic scleroderma involves connective tissues of the _____ and ________. Clinical features of this condition follow the acronym CREST which is what?

A

C: Calcinosis - calcium deposits in subQ tissue

R: Raynaud phenomenon (decreased blood flow in response to cold/stress)

E: esophageal changes (swallowing difficulty and fibrosis)

S: Sclerodactyly - tightening of skin over fingers and toes

T: telangiectasias - dilation of capillaries causing small weblike marks on skin surface

220
Q

Seborrheic keratosis is what?

A

benign proliferation of cutaneous basal cells with unknown pathogenesis

221
Q

Lesions of seborrheic keratosis present like what?

A

Lesions - vary in colour (tan to waxy yellow, could turn dark)
- oval and greasy looking lesions with hyperkeratotic scale

222
Q

Treatment of seborrheic keratosis includes what?

A
  • cryotherapy

- laser therapy

223
Q

Urticaria is associated with ________ hypersensitivity to allergens, and is caused by _______ release which causes leakage of fluid from the vessel and appears as wheals, welts, or hives.

A

type I; histamine

224
Q

Chronic urticaria presents as recurrent wheals over ____ weeks and major S/S is _______ (welts/swelling deeper within skn or mucous membranes) commonly affecting the eyes and mouth.

A

6; angioedema

225
Q

What is keratoacanthoma and usually occurs in who?

A

benign, self-limiting tumour of squamous cell differentiations arising from hair follicles

  • usually occurs of sun-damaged skin of elderly; highest incidence among males and smokers
226
Q

Treatment for keratoacanthoma?

A

can spontaneously resolve but can be removed to reduce it from turning into squamous cell carcinoma (SCC)

227
Q

What are scabies and how are they transmitted?

A

A contagious disease caused by itch mite which can colonize the epidermis. .

  • transmitted by close personal contact and by infected clothing/bedding
228
Q

Contributing factors to scabies include:

A
  • overcrowded housing
  • poor sanitation
  • being a child
229
Q

Characteristics of scabies on skin, and its treatment include what?

A

Characteristics:

  • tunnels under skin (burrows)
  • pruritis esp at night, papules, and vesicular lesions

Treatment
- scabicide, wash everything in hot cycles or dry cleaned

230
Q

Lice are parasites that survive on _____ and reproduce every ___ weeks. Lice bites secrete toxic saliva that produces _______ _______. Lice can be acquired by _______ contact.

A

blood; 2; pruritic dermatitis; direct

231
Q

Treatment for lice?

A
  • topical shampoo

- wash clothing and bedding

232
Q

Bedbugs are blood sucking parasites that are attached to _____ and _____. How long do they feed for before disappearing and bites are usually on what areas ?

A

Warmth, CO2

Feed for 5-15 minutes before disappearing

Bites are usually on areas not covered by clothing

233
Q

treatment for bedbug bites?

A
  • oral antihistamines

- topical corticosteroids

234
Q

What is actinic keratosis?

A

Premalignant lesions (i.e. precancer) that is composed of abnormal proliferations of epidermal keratinocytes due to prolonged UV exposure.

235
Q

What do actinic keratosis lesions look like and what is the treatment?

A

Lesions: tough, poorly defined papules with telangiectasia

Treatment: sun protection, cryoablation, laster surgery, photodynamic therapy, topical therapy

236
Q

What are nevi?

A

Moles/birthmarks (benign pigmented or non-pigmented lesions) formed from melanocytes

237
Q

Sort the following classifications of nevi from most likely to least likely to develop into melanoma.

1) junctional nevus
2) compound nevus
3) intradermal nevus

A

1) junctional nevus
2) intradermal nevus
3) compound nevus

238
Q

The most common type of cancer is ______ cancer and the most serious type of this cancer is _______ _______.

A

skin (but also basal cell carcinoma if you’re talking more specifically and not a general type of cancer), malignant melanoma

239
Q

Non-melanoma skin cancers include which two cancer types?

A
  • Basal cell carcinoma (BCC)

- Squamous cell carcinoma (SCC)

240
Q

BCC is caused by what factors (2)? If left untreated, what could happen?

A
  • UV radiation exposure
  • arsenic in food and water

If not treated, can invade surrounding tissues and destroy a nose, eyelid, or ear

241
Q

BCC lesions have varied presentations but generally will grow (quickly/slowly), often ulcerate and develop crusts, and metastasis is (rare/common).

A

slowly; rare

242
Q

What is squamous cell carcinoma (SCC)?

A

Tumour of the skin, second most common human cancer

243
Q

Causes of SCC include:

A
  • UV rays
  • high arsenic levels in drinking water
  • exposure to x-rays and gamma rays
  • immunosuppression
  • light coloured skin
244
Q

SCC is the most common cause of ____ cancer.

245
Q

What is cutaneous melanoma?

A

malignant tumour original from melanocytes (due to malignant degeneration of melanocytes); most serious skin cancer

246
Q

It is recommended to monitor nevi for potential of it becoming melanoma using the ABCDE rule. What is this rule? What other factors would you consider when assessing for malignant melanoma?

A 
A - asymmetry
B - border irregularity
C - colour variation
D - diameter larged than 6 mm
E- elevation/evolving

Other:

  • thickness of lesion (presence of tumor)
  • lymph node involvement
  • presence of metastasis
247
Q

What is kaposi sarcoma and what is it associated with?

A

Vascular malignancy associated with immunodeficiency; associated with human herpesvirus-8

248
Q

What are kaposi sarcoma lesions S/S?

A

pruritic, painful, purplish-brown lesions

249
Q

What is primary cutaneous lymphoma?

A

Primary cutaneous lymphomas are clonal expansions of T-cell and B-cell lymphocytes. Mycosis fungoides is the most common T-cell lymphoma.

250
Q

What is rubella?

A

A common communicable disease of children and young adults caused by a RNA virus that enters the bloodstream via respiratory route

251
Q

Rubella is (mild/moderate/severe) in most children and the incubation period is __ to ___ days. The rash itself lasts about ____ days. It is a (viral/bacteral/fungal) disease

A

mild; 14-21; 2-3 days; viral

252
Q

Prodromal symptoms of rubella include what? What symptoms present in children after prodromal period

A

Prodromal:

  • enlarged lymph nodes
  • low grade fever
  • headache
  • sore throat
  • rhinorrhea
  • cough

After: rash 1-4 days after onset of initial symptoms

253
Q

Rule of nines

A

Used to estimate TBSA

  • arm (each side is 4.5% so an entire arm front and back is 9%)
  • torso: 18% on each side
  • leg (each side is 9%, entire leg front and back is 18%)
  • head: front is 4.5% so entire head is 9%
  • genital region: 1%
254
Q

Identify the following for first degree burns:

1) Morphology of skin:
2) Pain/touch sensation:
3) Blisters:
4) Appearance of wound:
5) Healing time:
6) Scarring:
7) Treatment

A

1) epidermis affected only; some localized redness and swelling
2) intact pain sensation
3) no blisters
4) skin peels in 24-48 hours; slightly red underneath
5) heals in 3-5 days
6) No scarring
7) typically none (except for elderly and infants, may need fluid therapy)

255
Q

Identify the following for second degree burns (superficial partial thickness):

1) Morphology of skin:
2) Pain/touch sensation:
3) Blisters:
4) Appearance of wound:
5) Healing time:
6) Scarring:
7) Treatment

A

1) epidermis and some dermis destroyed
2) intact pain sensation (lots of pain!)
3) blisters form within minutes (thin walled, fluid-filled)
4) red to pale ivory with moist surface
5) heals in 21-28 days (3-4 weeks)
6) potential scarring (genetically based)
7) general wound care, do not pop blisters

256
Q

What exacerbates Candidiasis (9 risk factors)?

A

1) moisture, warmth, maceration, occlusion
2) systemic admin of antibiotics
3) pregnancy
4) DM
5) Cushing disease
6) debilitated states
7) infants <6 months (decreased immune reactivity)
8) immunosuppressed people
9) certain neoplastic diseases of blood/macrophage system

257
Q

Identify the following for second degree burns (deep partial thickness):

1) Morphology of skin:
2) Pain/touch sensation:
3) Blisters:
4) Appearance of wound:
5) Healing time:
6) Scarring:
7) Treatment

A

1) destruction of epidermis and dermis; skin appendages left
2) intact pain sensors but diminished (no glands and follicles involved)
3) Blisters - may or may not appear as fluid filled blisters (often flat, dehydrated paper-life skin tissue that lifts off in sheets)
4) mottled with areas of waxy, white, dry surface (minimal exudate)
5) 30 days to many months
6) slow healing so scarring is common (hypertrophic scarring)
7) surgery to remove necrotic tissue; potential autograft needed

258
Q

Identify the following for third degree/full thickness burn:

1) Morphology of skin:
2) Pain/touch sensation:
3) Blisters:
4) Appearance of wound:
5) Healing time:
6) Scarring:
7) Treatment

A

1) All layers destroyed - epidermis, dermis, and subQ tissue
2) no intact tactile/pain sensors
3) blisters - rare, flat dehydrated paper-like skin that lifts off easily
4) dry, hard, leathery surface; white, cherry red, or black; may have visible thrombosed veins
5) Healing - will not heal (may close from edges as secondary healing if it’s small wound)
6) skin graft needed; minimal scarring if early excision and grafting
7) escharotomies (tissue decompression) to prevent compartment syndrome

259
Q

Identify the following for fourth degree burn (full thickness + deeper tissue):

1) Morphology of skin:
2) Pain/touch sensation:
3) Blisters:
4) Appearance of wound:
5) Healing time:
6) Scarring:
7) Treatment

A

1) destruction of epidermis, dermis, subQ tissue, and tendons/muscle/bone
2) no intact tactile/pain sensors
3) no blisters
4) wound looks black and charred
5) healing - will not heal; skin graft required (potentially amputation or reconstructive surgery)
6) scarring - depends on success of surgery
7) Treatment: ^^ re: surgery

260
Q

Severity of burn depends on what factors?

A
  • age
  • medical hx
  • extent of injury
  • depth of injury
  • body area involved
  • TBSA
261
Q

Major burn injuries are those that are considered _____ % TBSA but a systemic hypermetabolic response is activated with a burn injury that is ____ % TBSA.

A

> 20 ; >30

262
Q

What happens to the body after a large serious burn? (2)

A

1) evaporative water loss
2) fluctuations of large amounts of fluid, electrolytes, and plasma proteins into body tissues (which looks like generalized massive edema, circulatory hypovolemia, hypotension)

263
Q

What is the immediate/acute systemic physiological consequence of a large serious burn?

A
  • increased capillary permeability leading to hypovolemic shock
  • cellular and immunologic disruption
264
Q

What is burn shock?

A

A condition characterized by decreased cardiac contractility and decreased cardiac output with inadequate capillary perfusion (decreased cardiac output due to myocardial depressant factor and reduced intravascular volume) - occurs during the first 24 hours

265
Q

Hypovolemia from burn shock results from what?

A

massive fluid losses and shifts to interstitial spaces from circulating blood volume

266
Q

What is the cardiovascular and systemic response to burn injury (4)?

A
  • decreased cardiac contractility
  • decreased cardiac output with inadequate capillary perfusion in tissues
  • fluid and protein move out of vasculature leading to elevated Hct and WBC count, and hypoproteinemia
  • capillary seal (endpoint of burn shock)
267
Q

What is the metabolic response to burn injury?

A
  • hypermetabolic response (increased energy expenditure, O2 consumption, hyperglycemia, insulin resistance, catabolic loss of muscle mass)
  • hyperdynamic circulation (abnormally increased circulatory volume)
  • increased thermal regulatory set point, core temp (tachy, hypercapnia, body wasting)
  • known as “flow phase” and this happens due to compensation for profound water and heat loss from burn (occurs ~48 hours after ebb phase)
268
Q

Treatment of burn injury to counteract metabolic response?

A
  • insulin therapy
  • increase ambient temperature
  • early excision/grafting to decrease resting energy expenditure
269
Q

What is ebb phase and when does it occur?

A
  • starts immediately and lasts for the first 24-72 hours after burn injury
  • increased vascular permeability
  • fluid shifts, edema (blood shunted away from kidney and gut)
  • hypodynamic circulation, hypometabolic state, decreased O2 consumption
270
Q

Treatment during ebb phase/resuscitation phase?

A

IV fluid resuscitation (ringer’s lactate) to restore blood volume (use Parkland or modified Brooke formula)

271
Q

What is the immunologic response to burn injuries?

A
  • immunosuppression after surviving burn shock (leading to increased susceptibility to sepsis)
272
Q

What is the response of water loss in burn injury?

A
  • dramatic increase in water loss due to loss of skin barrier function and ability to regulate evaporative water loss
  • also due to hyperventilation and hypermetabolism
273
Q

General burns management includes what?

A
  • wound debridement and closure; wound management
  • adequate fluids and nutrition
  • treatment for infection and sepsis
  • promotion of thermoregulation
  • tons of drugs
  • reconstructive surgery and escharotomies (skin grafts)
274
Q

What is the parkland formula?

A

TBSA x weight (in kg) x 4mL

  • 1/2 half in first 8 hours
  • 2nd half in next 16 hours
275
Q

Frostnip and S/S.

A

exposure to cold without tissue freezing; mild and completely reversible injury characterized by pallor and numbness

S/S ^ as mentioned above + redness and discomfort during rewarming, no tissue damage

276
Q

Chilblains and S/S.

A

Small lesions caused by the inflammation of tiny blood vessels after exposure to cold but no ice crystal formation

  • purple skin colour with plaques/nodules, pain, itching
277
Q

Frostbite and S/S

A

condition where tissues freeze and form ice crystal at temps below -2C (potentially reversible)

S/S:

  • white/yellowish with waxy texture
  • numbness and no pain sensation (and then severe pain when thawing)
278
Q

During rewarming in a frostbite injury, what conditions and S/S are considered/prsent?

A
  • progressive microvascular thrombosis followed by reperfusion injury with release of inflammatory mediators
  • impaired circulation and anoxia in exposed area
  • cyanosis, mottling, and then redness, edema, burning pain once rewarmed
279
Q

Outline frostbite classification and indicate which classification results in gangrene and tissue loss.

A

Based on depth of injury

First degree: superficial includes partial skin freezing

Second degree: full thickness skin freezing

Third degree: deep includes full thickness and subQ freezing

Fourth degree: deep tissue freezing

  • third and fourth degree result in gangrene and tissue loss
280
Q

What is flash freeze?

A

Rapid cooling with intracellular ice crystals associated with contact with cold metals or volatile liquids

281
Q

Treatment for frostbite includes what?

A
  • cover affected areas with other body surfaces and warm clothing
  • no rubbing or massaging
  • analgesics for pain
  • antibiotics
  • vasodilators
  • tissue debridement
282
Q

General hair loss from head or body is known as what? It occurs when there is a disruption to what?

A

alopecia; due to disruption in growth phase of hair follicle

283
Q

What is androgenic alopecia and it happens in 80% of which demographic?

A

localized hair loss, occurs in about 80% of men

284
Q

Cause of androgenic alopecia?

A

genetic predisposition to androgens causing androgen-sensitive hair follicles (on top) to turn into vellus follicles that grow short, thin hair

285
Q

Describe male-pattern baldness.

A

Begins with frontotemporal recession and then progresses to loss of hair over top of scalp

286
Q

Female-pattern alopecia involves ___ part of scalp and has usually no hair loss along ________ (front/side/back) hairline.

A

central, front

287
Q

Male-pattern and female-pattern alopecia are similar in that they both involve hair loss in the __________ area of the scalp, but male-pattern alopecia also includes the ____________ area.

A

central; frontotemporal

288
Q

What is alopecia areata and what is it caused by?

A

autoimmune T-cell mediated chronic inflammatory disease against hair follicles resulting in hair loss (usually in patches)

causes:

  • stressful events
  • metabolic disorders
  • genetic susceptibility
  • cell-mediated immune cytokines
289
Q

What is hirutism and whom does it commonly occur in?

A

Abnormal growth and distribution of hair on face, body, and pubic area and potentially frontotemporal hair recession; occurs in women

290
Q

What is hirutism caused by?

A

caused by high levels of androgen (and areas affected are androgen-sensitive areas)

291
Q

What is paronychia and what causes it?

A

acute/chronic infection of the cuticle due to frequent exposure to moisture allow bacteria or fungus to get in

292
Q

What are S/S and treatment for paronychia?

A

S/S for ACUTE paronychia - pain, inflammation of cuticle, abscess and pus, edema in skin around nail

Treatment: keep hands dry; topical therapy (oral antifungals don’t work)

293
Q

Onychomycosis is also known as _______ _______ and is a (fungal/viral/bacterial) infection of the nail unit.

A

tinea unguium; fungal

294
Q

What are S/S and treatment for onychomycosis?

A

S/S: nail plate turning yellow/white and becomes elevated due to hyperkeratotic debris within plate; no pitting on nail surface

Treatment: systemic antifungal drugs

295
Q

In elderly, what happens to skin integrity re the following?

1) thickness
2) moisture
3) elasticity
4) sensory perception
5) temp regulation

A

1) thin - leads to a host of different risks (increased permeability of things you don’t want in your body)
2) drier - atrophy of sebaceous and sweat glands
3) loss of elastin = more wrinkly and easy to tear
4) Decreased pressure/touch receptors and free nerve endings = reduced sesnsory perception
5) decreased temp regulation

296
Q

What are the three major muscle types?

A

1) skeletal (voluntary, striated muscles)
2) smooth (involuntary muscle)
3) cardiac (involuntary, striated muscles)

297
Q

How many bones in the body?

298
Q

Osteoblasts vs osteoclasts vs osteocytes.

A

Osteoblasts: rebuild new bone by synthesizing collagen and proteoglycans and mineralizing osteoid matrix

Osteoclast: reabsorbs bone material from old/excess bone

Osteocytes: osteoblasts that are diffentiated and no longer build bone but they do communicated with osteoblasts/osteoclasts about when and where to form and resorb bone

299
Q

________ can differentiate into multiple cell types, including osteoblasts and osteocytes.

A

mesenchymal stem cell lineage

300
Q

Mesenchymal stem cells in bone marrow develop into (blood cells, tissue cells such as fibroblasts).

A

tissue cells such as fibroblasts

301
Q

Osteoclasts original from _______ stem cells.

A

hematopoietic

302
Q

Axial vs appendicular skeleton. # of bones and bones involved.

A

Axial: 80 bones, skull, vertebral column, thorax

Appendicular: 126 bones, upper and lower extremities, shoulder girdle, pelvic girdle

303
Q

Compact bone is also called _____ and accounts for ___ % of the skeleton. Spongy bone is also called ______ and accounts for ___ % of the skeleton. Both of these tissues are present in every bone.

A

cortical; 85%

cancellous; 15%

304
Q

Compact bones is extremely strong and highly organized with something known as a ________ system.

305
Q

What does the Haversian system do and what is it composed of?

A

series of tubes that allow for blood vessels and nerve to travel through

Each canal has:

1) capillaries and nerves
2) Haversian canal (central canal)
3) Lamellae (concentric layers of bone matrix)
4) Lacunae (tiny spaces between lamellae)
5) Osteocytes in lacunae
6) Canaliculi - canals for communication

306
Q

Spongy bone contains an irregular meshwork known as ________ with red bone marrow filling the spaces in between.

A

trabeculae

307
Q

Periosteum

A

double layered connective tissue that covers ALL bones and has blood vessels/nerves

308
Q

The collagenous fibers that anchor bone to the inner layer of the periosteum as well as anchoring tendons/ligaments to periosteum is known as what?

A

Sharpey fibers

309
Q

Diaphysis vs metaphysis vs epiphysis

A

Diaphysis - main shaft
Metaphysis - broader neck
Epiphysis - broad end of bone

310
Q

Definitions of each:

1) Long bones
2) Flat bones
3) Short bones
4) Irregular bones

A

1) Long bones - longer than they are wide and narrow tubular mid portion
2) Flat bones - two plates of compact bone nearly parallel to each other with a layer of spongy tissue in between
3) Short bones - often cuboidal, spongy bone with thin outer layer of compact bone
4) irregular bones: various shapes that are both thin/thick

311
Q

What are the 5 stages of bone healing and their timeframes?

A

1) inflammation/hematoma formation (occurs within hours of injury/surgery)
2) procallus formation (by osteoblasts) - within days
3) callus formation - within weeks
4) replacement of bone by multicellular units - years
5) remodeling of periosteal and endosteal surfaces of the bone to pre-injury shape and size - years

312
Q

Primary function of joints

A

to provide stabiliy and mobility to the skeleton

313
Q

What are the classifications of joints based on their movements? 3 types and give examples of each.

A

1) synarthrosis: immovable joints so no movement (ex. joints between skull bones)
2) Amphiarthrosis: slightly moveable joint so some movement (ex. vertebrae joints)
3) Diarthrosis: freely moveable (ex. ankle, wrist, knee, hip, shoulder)

314
Q

What are the classifications of joints based on connective structures?

A

1) fibrous
2) cartilaginous
3) synovial (condyloid, gliding, hinge, pivot, saddle, ball and socket)

315
Q

Substance that gives synovial fluid its viscous quality is called what?

A

hyraluronate

316
Q

What cells secretes hyaluronate into joint fluid.

A

synovial fibroblasts (B cells)

317
Q

What cells secrete collagen and other components of cartilage, and maintain the cartilaginous matrix?

A

Chondrocytes

318
Q

Articular cartilage is a layer of _____ cartilage that covers the ends of each bone. Its function is to do what?

A

hyaline

function: to reduce friction in joint and distribute weight-bearing forces

319
Q

Fibrous joints vs. cartilaginous joints

A

fibrous: joints where bones attached together by fibrous tissue, has no joint cavity, and allows little to no movement
cartilaginous: joints where bones are joined by cartilage, allows some movement

320
Q

What are the fibrous joint subtypes?

A

1) Sutures: binds interlocking flat bones
2) Syndesmosis: joint where two bony structures united by ligament/membrane
3) Gomphosis: specialized peg/socket joint held in place by a ligament (ex. teeth held in maxilla/mandible)

321
Q

What are the cartilaginonus joint subtypes

A

1) symphysis: bones are attached by pad/disk of fibrocartilage and articulating surfaces covered by hyaline cartilage
2) synchondrosis: hyaline cartilage connects two bones (rather than fibrocartliage)

322
Q

Joint/articular capsule vs joint/synovial cavity.

A

Joint capsule: fibrous connective tissue that covers the bone ends at a joint

Joint cavity: a fluid filled space between the articulating surfaces of two bones

323
Q

Composition and function of synovial fluid

A

Composition: superfiltrated plasma from blood vessels (contains hyaluronic acid, synovial cells, and leukocytes)

Function:

  • lubricates joint surfaces
  • nourishes pad of articular cartilage
  • covers bone ends
324
Q

Bursae vs. tendon vs ligament.

A

Bursae: small sacs of synovial fluid

tendon: bands of fibrous connective tissue attaching muscle to bone

Ligaments: bands of tissue to connect bone to bone

325
Q

What happens to bones as we age?

A
  • loss of bone tissue and they become less dense, less strong, and more brittle
  • bone remodeling takes longer
326
Q

Between men and women, who experiences bone loss at later ages and at much slower rates?

A

men (they also have more initial more bone mass, about 30%)

327
Q

What happens to our joints as we age?

A
  • cartilage becomes more rigid, fragile, and susceptible to fraying (due to decreased water content, sugar concentrations, more collagen-elastin bonds)
  • decreased ROM
  • prone to fractures
  • cartilage disk spaces decrease so we get shorter
  • tendons shrink and harden
328
Q

What happens to our muscles when we age?

A
  • decrease in mass and strength
  • less mitochrondria, smaller motor units, reduced RNA synthesis
  • decrease max oxygen consumption, metabolic rate is reduced
329
Q

What is the most common disease affecting bone?

A

osteoporosis

330
Q

What is a fracture and when does it occur?

A

A break in the continuity of a bone, occurs when the force applied exceeds tensile or compressive strength of the bone

331
Q

Complete vs incomplete fracture

A

Complete: bone broken entirely

Incomplete: damaged but still in one piece (tends to occur in children because more flexible growing bones)

332
Q

When does a open fracture occur (i.e. cause)?

A

Moderate to severe energy that is continuous and exceeds tissue tolerance

333
Q

What is a comminuted/segmented fracture and what caused it?

A

The bone that breaks into more than two fragments

cause: Direct or indirect to moderate/severe force

334
Q

What is a linear fracture?

A

A fracture that runs parallel to the long axis of bone

335
Q

What is an oblique fracture and what causes it?

A

A fracture of a slanted angles across the shaft of the bone impacting both cortices

cause: Direct or indirect energy with angulation and some compression

336
Q

What is a spiral fracture and what caused it

A

A fracture that occurs around cortices and may becomes displaced by twisting

cause: Direct or indirect twisting energy/force with the distal part held or unable to move

337
Q

What is the transverse fracture and what causes it?

A

A fracture that straight across the bone

cause: Direct or indirect energy towards the bone

338
Q

What is an occult fracture and when does it occur?

A

Fracture that is hidden and not readily discernible

Cause: minor force or energy

339
Q

What is a pathologic/fragility fracture and what causes it?

A

A fracture of the bone that is weakened by the presence of a tumour or pressure of an abnormality

Cause: could be minor force or energy but can also occur with normal weight bearing activities because the bone lacks a normal ability to deform and recover

340
Q

What is a greenstick fracture and what is the cause?

A

Break in only one cortex of the bone splintering spongy bone (basically the outer surface is disrupted but the inner surface remains intact)

cause: minor direct or indirect energy

341
Q

What is an impacted fracture and what causes it?

A

A fracture with one side wedged into the inside of the other fragment (basically one side of the bone fragment is tunneled into the other)

Cause: compressive axial energy or force directly to the distal fragment

342
Q

What is a torus fracture?

A

Incomplete fracture - Buckling of the cortex of a bone but does not break

343
Q

What is a bowing fracture and what causes it?

A

Incomplete fracture - bending of bone usually due to longitudinal force applied to it

344
Q

What is a stress fracture and what causes it?

A

microfractures caused by repeated strain

  • consists of fatigue fractures which are usually in people who are new to activity and overdo it - gets shin splints that turn into stress fractures)
  • pain occurs with activity, relieved with rest
345
Q

What is a transchondral fracture?

A

fragmentation and separation of a portion of cartilaginous joint surface (articular cartilage) from main shaft of bone

  • limited ROM, may have crepitus/audible clicking sounds
346
Q

What is an avulsion fracture? It is a type of (complete/incomplete) fracture.

A

Complete fracture

- fragment of bone connected to a ligament or tendon detachs from main bone

347
Q

What is a compression fracture? It is a type of (complete/incomplete) fracture.

A

Complete fracture

- fracture wedged or squeezed together on one side of the bone

348
Q

What is a displaced fracture?

A

Fracture with one, both, or all fragments out of normal alignment (basically could be any one of the other fracture types as long as the fragments are not aligned anymore)

349
Q

Extrascapular vs intrascapular fracture

A

Extrascapular: fracture close to joint but remains outside joint capsule

Intrascapular: fragment within joint capsule

350
Q

What happens during direct/primary healing of the bone?

A

intramembranous bone formation occurs when adjacent bone cortices are in contact with one another (i.e. surgery fixation devices); no callus formation

351
Q

What happens during indirect (secondary) healing? When does this occur?

A

intramembranous and endochondral bone formation occurs (i.e. bone develop from fibrous tissue and hyaline cartilage), callus forms, and bone remodelling

  • happens when using a cast or non-surgical method
352
Q

_____ and ______ do not result in scar tissue after healing

A

Bone, liver

353
Q

What are the 5 stages in bone healing?

A

1) bleeding at fragment ends leading to hematoma formation
2) hematoma organized into fibrous network
3) osteoblasts invade, collagen strands lengthened, calcium deposited
4) callus formation (new bone built while old bone destroyed)
5) remodeling is done while excess callus is reabsorbed and trabecular bone deposited along lines of stress

354
Q

Difference: Traction via skin traction & via skeletal traction.

A

Skin traction: a few pounds of pulling force needed to realign fragments (temporary traction)

Skeletal traction - actually using pins and wires drilled through bone to hold traction

355
Q

Internal fixation

A

Hardware used to manipulate fragments back into alignment (surgical)

356
Q

External fixation

A

pins and rods are surgically placed into uninjured bone near fracture site and stabilized with external bar frames

357
Q

Improper reduction/immobilization can lead to:

1) nonunion
2) delayed union
3) malunion

What do each of these mean?

A

1) nonunion: failure of bone ends to grow together, the gaps end up being filled with dense fibrous and fibrocartilaginous tissue instead of bone - may create a false joint/pseudoarthritis
2) delayed union: union that does not occur until approx. 8-9 months after a fracture
3) malunion: healing of bone in an incorrect anatomical position

358
Q

Dislocation vs subluxation

A

dislocation: displacement of one or more bones in a joint in which the opposing joint surfaces entirely lose contact with one another
subluxation: partial loss of contact between two opposing joint surfaces

359
Q

Most common joint dislocations/subluxations are? (6)

A

1) shoulders (glenohumeral joint)
2) elbows - nursemaid’s elbow
3) wrists - any one of the 8 carpal bones
4) fingers - usually MCP (knuckles) and PIP (fingers) joints
5) knee - due to this being an unreliable weightbearing joint
6) hip - posterior dislocations common (in MVCs)

360
Q

Describe the cause for each of the following clinical manifestations of dislocations/subluxuations.

1) pain
2) swelling
3) limited ROM
4) joint deformity

A

1) caused by effusion of inflammatory exudate (fluid leaking into affected area)
2) swelling - see above ^
3) limited ROM - from effusion into joint
4) from muscle contractions that exert pull on joint

361
Q

Reduction and immobilization of the joint for ____ (range) weeks to allow healing of damaged structures, followed by exercises to restore ROM.

362
Q

Tendons (facilitate/limit) movement while ligaments (facilitate/limit) movement.

A

facilitate; limit

363
Q

An area of attachment on the bone by the tendon is called?

364
Q

Difference between sprains and strains?

A

sprains: ligament rupture/tear

Strains: muscle/tendon tear/rupture

365
Q

What is the classification for sprains/strains? (3)

A

First degree: mild - fibers are stretched but muscle/joint remains stable

Second degree: moderate - incompelte tearing of fibers resulting in muscle weakness and some joint instability

Third degree: severe: full tears, muscle cannot contract normally and ++ joint instability

366
Q

A healing tendon/ligament lacks sufficient strength to withstand stress for _____ weeks after injury

367
Q

How do sprains/strains heal?

A

collagen formation begins 4-5 days after injury and eventually the tissue fuses the new and surrounding tissues into a single mass (and tendon gets reconnected with the bone)

mechanical stability of a joint eventually achieved at 3 month mark

368
Q

Treatment for strains/sprains include the acronym PRICE. what does it stand for?

A 
Protection
Rest
Ice
Compression
Elevation

for 72 hours

369
Q

Tendinopathy vs. epicondylopathy.

A

Tendinopathy: tissue degradation and irritation of a tendon (book says it’s “inflammation” of a tendon

Epicondylopathy: “inflammation” of a tendon where tendon/ligament attachs to the bone

370
Q

Tennis elbow vs. golfer’s elbow

A

Tennis elbow: aka lateral epicondylopathy

  • irritation and overstetching of ECRB tendon + foraem extensor muscles
  • leads to loss of grip strength and pain

Golfer’s elbow: aka medial epicondylopathy
- irritation and overstretching of forearm muscles that are involved with flexion and pronation

371
Q

Joint movement is compromised in bursitis. True or False

A

False - bursae lie outside of joints so joint movement is not compromised

372
Q

What is the cause of bursitis?

A

inflammation due to overuse or excessive pressure, but could also be from:

  • infection
  • autoimmune diseases
  • crystal deposition
  • acute trauma
373
Q

What is a muscle strain and what is it caused by?

A

general term for local muscle damage, caused by sudden forced motion causing muscle to be stretched beyond normal capacity

374
Q

What are the three phases of muscle healing?

A

1) Destruction - myofibers of damaged muscle contract and necrose
2) Repair - dead cells phagocytosed and myoblasts go to injury site

both ^ occur within the first week of injury

3) Remodeling - myofibers mature to form contractile tissue and attach to ends of scar tissue (up to 6 weeks)

375
Q

Degrees of muscle strain and respective tx for such.

A

1) first deg:
- muscle overstretched, pain but no muscle deformity
- tx: ice 5-6x (within first 24-48 hours) and then gradually resume full weight bearing after 2 weeks of rest

2) second degree:
- muscle intact with some fiber tearing, swelling, and pain
Tx: similar to first degree

3) third degree:
- caused by tearing of fascia, marked weakness, deformity
- tx: surgery, immobilization, and non-weight bearing for 6 weeks

376
Q

Myositis/heterotopic ossificans

A

a late complication of some muscle injuries that occurs when bone or bone-like tissue grows where it’s not supposed to (cell differentiation is all screwed up)
- leads to stiffness and deformity of an extremity

377
Q

What is rhabdomyolysis?

A

disease involving rapid breakdown of muscle that causes release of intracellular contents including myoglobin into extracellular space and bloodstream

378
Q

What is happening in the disease process of rhabdomyolysis?

A

1) After major injuries/trauma, skeletal muscles are injuried causing ischemia and necrosis and then lots of swelling occurs and bunch of stuff gets pushed out from the muscle cells (myoglobin, potassium, and creatine kinase (CK))
2) leads to hyperkalemia, cardiac arrythmia, and acute renal failure

379
Q

S/S of rhabdomyolysis?

A
  • classic triad: muscle pain, weakness, and dark urine

- others: fever, malaise, nausea/vomiting, confusion, agitation, delirium, anuria

380
Q

Contributing factors to rhabdomyolysis? (7 categories)

A

1) direct trauma (like crush injuries)
2) drugs
3) excessive muscular contraction (like epilepsy or ++ strenuous exercise)
4) Infectious agents (viral, fungal, or bacterial)
5) Toxins (CO, insect toxins)
6) Hereditary enzyme disorders
7) misc. causes: heat/cold related, electrolye disorders

381
Q

True or False. In rhabdomyolysis, risk of renal failure increases proportionally with increase in levels of serum CK, K, and potassium

A

True (CK levels are off the charts) - renal failiure likely when CK reaches 15 000 units/L

382
Q

What are the priority goals of treatment in rhabdomyolysis? How is this achieved?

A

preventing renal failure and maintaining adquate urinary output

  • IV fluids and rest; possibly temporary dialysis for hyperkalemia
383
Q

What is Osgood-Schlatter disease?

A

Disease caused by insufficient blood supply to the bones (osteochondroses) of the tibia tubercle (shin) and is associated with patellar tendonitis

384
Q

Osgood-Schlatter disease is common in which demographic and S/S include what?

A
  • preadolescents/adolescents who play sports, more common in males
  • varying severity (from mild tendonitis to tibial apophysis separation)
  • pain, swelling in patellar region and just below it + tenderness
  • Sx more severe after quad-dominant movements (jumping/running) or direct trauma to the area
385
Q

Treatment for Osgood-Schlatter disease?

A
  • goal: decrease stress at the tubercle
  • 4 to 8 weeks restriction from strenuous physical activity
  • antiinflammatory meds
  • stretching of quads
  • potential brace/cast
386
Q

What is osteogenesis imperfecta (OI)?

A
  • aka brittle bone disease

- disease related to abnormal growth of bones related to collagen

387
Q

How does osteogenesis imperfecta clinically manifest?

A
  • osteopenia (Decreased bone mass)

- increased rate of fractures

388
Q

Which type of scoliosis is most common?

A

idiopathic (type of structural scoliosis

389
Q

What does osteogenesis imperfecta cause?

A
  • increased fractures risk
  • abnormal dentition (arrangement of teeth)
  • basically things that can be caused by ++bone fragility
390
Q

What is compartment syndrome?

A

Condition caused by increased pressure within a muscle compartment

391
Q

What does compartment syndrome result in?

A
  • Fascia not being able to expand

- diminished capillary blood flow meaning local tissue hypoxia and necrosis

392
Q

Three general factors of compartment syndrome include:

A

1) conditions that increase compartment contents (bleeding, edema)
2) decrease in compartment’s physical volume (tight bandage, cast)
3) disruptions in vascular supply to an extremity increasing pressure within compartment (burns, insect bites, crush injuries)

393
Q

Diagnosis of compartment syndrome involves a clinical exam and 6P’s. What are the 6P’s?

A

1) Pain - out of proportion to injury (esp. with passive extension of fingers/toes)
2) pressure: swelling/rigidity in affected area
3) Pallor: pale
4) paresthesia: impaired sensation to are
5) Paresis: impaired function of involved extremity
6) pulselessness: loss of pulse to the area

394
Q

If left untreated, compartment syndromes can lead to what?

A

Volkmann Ischemic Contractures

395
Q

What is malignant hyperthermia?

A

Autosomal dominant muscle disorder characterized by hypermetabolic reaction to certain voltaile anesthetics or depolarizing muscle relaxants (due to mutation in RyR1 receptor)

396
Q

How does Malignant Hyperthermia manifest? Treatment?

A
  • mutations cause calcium release so continuous muscle contraction
  • hypermetabolism leading to ++high body temp, muscle rigidity, rhabdo, and death

tx: muscle relaxant (dantrolene)

397
Q

Dx and Tx for malignant hyperthermia

A

Dx: gathering hx, caffeine halothane muscle contracture test

Treatment: dantrolene (muscle relaxer)

398
Q

Osteoporosis

A

Official definition: a systematic skeletal disease characterized by low bone density and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility

basically: Old bone is being resorbed faster than new bone being formed = decreased density, becoming thinner and more porous

399
Q

True or false. Osteoporosis is a consequence of the aging process.

A

False, old peeps can be super healthy at 100 with no osteoporosis

400
Q

Most common sites for osteoporosis related fractures (3)

A

spine, femoral neck, wrist

401
Q

Factors contributing to osteoporosis?

A
  • abnormal BMI
  • lack of sex hormones
  • vitamin D deficiency
  • hormones
  • medications
  • low physical activity
  • Low calcium intake
  • High % of lactose intolerance
  • Increased prevalence of diseases (sickle cell, lupus)
402
Q

Dx and Tx of osteoporosis?

A

Dx:

  • measuring bone mass density (dual xray absorptiometry -DXA)
  • other scans and measurements

Tx: risk reduction, fracture prevention

  • bisphosphonates (reduces bone resoprtion)
  • parathyroid hormone
403
Q

Postmenopausal osteoporosis

A

bone loss in middle-aged and older women due to estrogen deficiency or from estrogen-independent age related mechanisms

404
Q

Secondary osteoporosis

A

osteoporosis caused by other conditions

405
Q

regional osteoprosis

A

osteoprosisi confined to a segment of the appendicular skeleton, often no known cause but could be from things like disuse/immobilization

406
Q

Glucocorticoid-induced osteoporosis

A

most common cause of secondary osteoporosis

Corticosteroids tend to both reduce the body’s ability to form bone and increase how fast bone is broken down.

407
Q

S/S of osteoporosis

A
  • fractures
  • pain and bone deformity (from fractures)
  • kyphosis/Dowager’s hump
408
Q

Osteomalacia

A

metabolic disease characterized by inadequate and delayed mineralization of osteroid in mature bone - leading to soft bones

(aka normal remodeling but mineral calcification and deposition do not occur)

409
Q

Rickets

A

a condition that affects bone development in children; similar to osteomalacia in pathogenesis but occurs in growing bones of children

410
Q

The most important factor contributing to osteomalacia:

A

vit D deficiency

411
Q

Disease process of osteomalacia

A

lack of vit D = decreased plasma calcium concentration (because calcium can’t be absorbed without vit D) = mineralization does not occur

412
Q

S/S of osteomalacia

A
  • muscular/skeletal pain, weakness, and tenderness
  • hesistancy to walk
  • waddling gait
  • facial deformities
  • bowed legs/knock knees
  • fragility fractures
  • uremia
413
Q

Paget Disease (osteitis deformans)

A

condition characterized by localized abnormal and excessive bone remodeling (excessive resorption of spongy bone and deposition of disorganized bone)

(second most common bone disease after osteoporosis)

414
Q

What does Paget cause?

A

enlargement and softening of affected bones causing bowing deformity, fracture, or neurological problems

415
Q

S/S paget disease

A

usually asymptomatic but x-rays will show abnormal bone formation
- bone and joint pain

416
Q

Osteomyelitis

A

bone infection most often caused by bacteria

417
Q

Hematogenous osteomyelitis

A

bone infection caused by pathogens carried through the bloodstream

418
Q

Contiguous osteomyelitis

A

when infection spreads to adjacent bone (often caused by fractures penetrating wounds, surgical procedures)

419
Q

Contributing factors of osteomyelitis?

A
  • metabolic and vascular diseases
  • lifestyle risks (drug use)
  • advanced age
420
Q

Disease process of osteomyelitis.

A

1) invading pathogen provokes intense inflammatory response
2) reduced osteoblast activity, enhanced osteoclast activity leading to imbalance
3) small terminal vessels clot and exudate clogs bone’s caniliculi
4) blood supply cut off - necrosis and death
5) infection increases pathologic fractures; OR layer of new bone growth in children

421
Q

Sequestrum vs. involucrum

A

sequestrum - area of devitalized bone

involucrum - layer of new bone growth around existing bone

422
Q

Osteomyelitis can be acute, subacute, and chronic. Indicate the time frame of each of these subtypes of ostemomyelitis.

A

Acute: osteomyelitis diagnosed within 2 weeks after symptom onset (abrupt inflammation onset)

Subacute: disease has been present 1 to several months, vague S/S

Chronic: months to years; infection silent between exacerbations

423
Q

S/S osteomyelitis

A
  • Brodie abscess
  • rapid onset of sudden pain in affected bone
  • tenderness, swelling, heat, guarding, restricted movement
  • fevers/chills
424
Q

Osteoarthritis (OA) vs. rheumatoid arthritis (RA)

A

OA = loss/damage to articular cartilage, new bone formation of joint margins (osteophytes) - typically more due to mechanical wear and tear

RA: autoimmune disease distinguished by joint swelling and tenderness + destruction of synovial joints

425
Q

S/S of osteoarthritis

A
  • pain that worsens with activity and at night
  • stiffness that goes away after few minutes of movement
  • Heberden and bouchard’s nodes (bony enlargments)
  • pain, swelling, tenderness, limited ROM
426
Q

Risk factors of rheumatoid arthritis

A
  • geographic area of birth
  • diet
  • SES
  • smoking
  • strong genetic predisposition
427
Q

S/S of rheumatoid arthritis

A
  • widespread symmetric joint swelling
  • immobile joint from pannus formation
  • skin over joint may have ruddy, cyanotic hue and look thin/shiny
  • stiffness lasts ~1hr after rising in the morning
428
Q

Ankylosing Spondylitis (AS)

A

chronic inflammatory joint disease with stiffening and fusion (ankylosis) of spine and sacroiliac joints

429
Q

What is the disease process of ankylosing spondylitis?

A

excessive bone formation occuring at the enthesis (point where ligaments, tendons, and joint capsule insert into bone) resulting in fibrosis, ossification, and joint fusion

430
Q

Where does anykylosing spondylitis affect first?

A

sacroiliac joint

431
Q

What do the vertebral bodies look like in anykylosing spondylitis ?

A

square shape, “bamboo spine” (due to calcification of spinal ligaments)

432
Q

S/S anykylosing spondylitis .

A
  • initial low back pain and stiffness
  • early morning stiffness
  • painful forward flexion, rotation, and lateral flexion of spine
  • kyphosis
  • inflammation all over the body
433
Q

What is gout?

A
  • inflammation due to excessive quantities of uric acid in blood (hyperuricemia) and in other body fluids (overproduction and under excretion of uric acid)
434
Q

uric acid build up leads to formation of _________ crystals in and around joints

A

monosodium urate

435
Q

Gouty arthritis

A

prolonged accumulation of MSU crystals resulting in joint damage

436
Q

Tophi

A

small, white nodules formed with crystal deposition in subcutaneous tissues

437
Q

Who gets gout?

A
  • middle aged males who have high intake of alcohol, red meat (purine-rich foods), and fructose
438
Q

Manifestation of gout occurs in three stages:

A

1) asymptomatic hyperuricemia (no sx but elevated serum urate levels)
2) acute gouty arthritis - attacks to the joint
3) tophaceous gout - chronic stage of disease where tophi appear

439
Q

Contractures

A

Lack of full passive ROM of a joint due to muscle/soft tissue limitations

440
Q

Physiologic vs Pathologic contracture

A

physiologic: occurs in the absence of muscle action potential in muscle membrane (pump fails even though there’s plenty of ATP)
pathologic: permanent muscle shortening due to muscle spasm or weakness (even though lots of ATP and normal action potential but still not working)

441
Q

Fibromyalgia

A

chronic MSK syndrome characterized by diffuse joint and muscle pain, fatigue, and tender points

442
Q

S/S fibromyalgia

A
  • no systemic/localized inflammation
  • presence of fatigue
  • nonrestorative sleep
  • anxiety and depression
  • diffuse chronic pain (burning/gnawing)
  • widespread tenderness in all body regions
  • increased sensitivty to heat, cold, and electrical stimuli
443
Q

How is fibromyalgia diagnosed?

A
  • differential diagnosis from other conditions
  • questionnaires and scale re: pain and symptom severity
  • Sx being present at a similar level for at least 3 months
444
Q

Chronic Fatigue Syndrome

A
  • aka myalgic encephalomyelitis
  • chronic disease characterized by profound fatigue, MSK pain, cognitive impairment, unresful sleep (major hallmark), immune and energy production impairments
445
Q

Dx and Tx for Chronic Fatigue syndrome

A

Dx: cannot be objectified with lab testing

Tx: management and adapting to stressors, improve physical activity

446
Q

Disuse Atrophy

A

reduction in normal size of muscle fibers after prolonged inactivity from best rest, trauma (casting), or local nerve damage

447
Q

Someone on bed rest likely loses muscle strength from baseline levels at a rate of ____ %/day

448
Q

Toxic myopathy

A

muscle damage caused by drugs/toxins

449
Q

Most common cause of toxic myopathy

A

alcohol abuse

450
Q

Myotonic channelopathy

A

delayed muscle relaxation after voluntary muscle contractions leading to disabling muscle stifness and weakness

451
Q

Periodic paralysis

A

group of muscle diseases presenting with episodes of flaccid weakness due to depolarization of muscle membrane being severe enough that muscle cannot be fired again

452
Q

McArdle’s Disease

A
  • glyocogen storage disease - caused by inability to metabolize glycogen
453
Q

In McArdle’s Disease, discomfort is usually alleviated with rest and then they can resume exercising with little or no discomfort. This is known as ______.

A

second wind

454
Q

Pompe disease

A
  • aka acid maltase deficiency

- inability to break down glycogen effectively leading to accumulation of glycogen in cells in lysosomes

455
Q

Lipid deficiences are disorders that have abnormalities in ______ and ______ of fatty acids for energy. Deficiency is caused by ____ enzyme.

A

transporting and processing

CPT enzyme

456
Q

Tuberculosis, sarcoidosis, Tichinellosis, toxoplasmosis, and Staph. aureus are all examples of what set of disorders?

A

viral, bacterial, and parasitic myositis

OCHT Term I (14 decks)

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