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Clin med 1 > Dermatology-Peckham 2 > Flashcards

Dermatology-Peckham 2 Flashcards

1
Q

What is a common pruritic inflammatory disease of skin, mucous membranes and hair follicles?

A

Lichen Planus

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2
Q

What are the 4 Ps involving Lichen Planus?

A

Purple, Polygonal, Pruritic, Papule

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3
Q

Where are the lesions grouped to in lichen planus?

A

Flexor aspect of wrists, lumbar area, eyelids, shins, scalp

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4
Q

Si/sx of Lichen Planus

A

Pruritic, lesions appear for <1yr, can cause hair loss and damage nails. Variations can be ulcerative

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5
Q

Potent topical steroids w/occlusion is the proper tx for what?

A

Lichen Planus

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6
Q

What can also be known as a benign “warty” growth

A

Seborrheic Keratosis

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7
Q

Seborrheic keratosis has what presentation?

A

“Stuck on” flat or raised papule or plaque. White, flesh colored to tan, brown, warty or smooth

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8
Q

Is tx required for seborrheic keratosis?

A

No

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9
Q

What is a vascular neoplasm brought on by genetic factors, hormonal factors, immunodeficiency or infection with HHV-8?

A

Kaposi Sarcoma

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10
Q

What are the 4 types of Kaposi Sarcoma?

A
  1. Classic
  2. HIV associated
  3. Endemic/African
  4. Iatrogenic
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11
Q

Kaposi Sarcoma presentation

A

Purplish macules that evolve to infiltrative plaques and nodules or tumors, often on lower extremities with lymphedema

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12
Q

Where can Kaposi Sarcoma also involve?

A

GI tract and lungs (very rarely)

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13
Q

What is the best Dx for Kaposi Sarcoma?

A

Biopsy

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14
Q

What progresses slowly with rare lymph node or visceral involvement?

A

Kaposi sarcoma

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15
Q

Some treatment options for Kaposi sarcoma include?

A

Radiation therapy, cryotherapy, surgical excision of individual nodules, topical Alitretinoin, dye laser

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16
Q

What are in situ dysplasias resulting from UV radiation that may progress to SCC?

A

Actinic Keratosis

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17
Q

What is the most common epithelial precancerous lesion?

A

Actinic keratosis

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18
Q

Who is at greater risk for actinic keratosis?

A

White men older then 50 with an outdoor lifestyle

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19
Q

The etiology of actinic keratosis

A

UVR leads to mutations in TP53 and deletion of the gene coding for p16 tumor suppressor protein

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20
Q

What is the pathophys behind actinic keratosis?

A

Epidermal lesion with atypical keratinocytes at basal layer that can extend upwards

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21
Q

Where is actinic keratosis most commonly found on the body?

A

Chronically sun exposed surfaces like the face, ears, scalp, dorsal hands, forearms, anterior legs

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22
Q

On palpation, what does actinic keratosis feel like?

A

Sandpaper texture, most times more easily felt than seen

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23
Q

Actinic keratosis clinical manifestations

A

Multiple discrete, flat or elevated verrucous or keratotic, red, pigmented or skin colored

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24
Q

What would be some differential diagnoses for actinic keratosis?

A

BCC, SCC, seborrheic keratosis, lupus

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25
Q

Is is appropriate to biopsy for actinic keratosis?

A

Yes, clinical/history Dx is also very important

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26
Q

Treatment for actinic keratosis is

A

Surgical: cryotherapy
Medical: Imiquimod or 5-FU

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27
Q

Is cryotherapy effective with actinic keratosis?

A

Yes with limited lesions. Goal is to produce cell death at -320F

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28
Q

What structures in the skin are more resistant to cryotherapy?

A

Collagen, blood vessels and nerves are more resistant that keratinocytes

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29
Q

What is the risk for cryotherapy?

A

Blistering, melanocytes are more sensitive so if often leaves hypopigmented spots

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30
Q

Imiquimod

A

For extensive broad and numerous AK lesions. its an interferon inducer that produces an immune rxn against lesion

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31
Q

What does imiquimod cause?

A

Erythema and crusting, but is less irritating than 5-FU

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32
Q

5-FU

A

Interferes with DNA synthesis, apply bid for 4 weeks

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33
Q

Ingenol mebutate

A

Used for AK, induces cell death. Apply daily x 3 days to face or 2 days to body

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34
Q

How should you follow up on a pt with AK?

A

Areas should smooth over, stubborn lesions should be biopsied for concern for squamous cell carcinoma

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35
Q

How is the prognosis for pts with AK?

A

Good with continued monitoring every 2-6 mos

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36
Q

How can a pt prevent AK?

A

Avoid sun exposure, use broad spectrum sunscreen, apply often

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37
Q

What are the most common form of all cancers?

A

Nonmelanoma skin cancers

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38
Q

What type of cancer is an epithelial tumor of the basal keratinocytes?

A

Basal Cell Carcinoma

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39
Q

Who has a greater risk for BCC?

A

Same as AK, white men 40 yrs or older with an outdoor lifestyle

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40
Q

What are some causes for BCC?

A

UVR, immunosuppression for organ transplant increases risk as well

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41
Q

What does BCC arise from?

A

Immature pluripotential cells associated with the hair follicle

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42
Q

BCC lesions

A

Flat, firm, pale area that is small, raised, pink or red, translucent, pearly and waxy, and the area may bleed following minor injury. May have “rolled edge”

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43
Q

A lesion that bleeds without significant pain or symptoms can be from what?

A

BCC

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44
Q

What is nodular BCC?

A

Most common, waxy, pearly, semitranslucent nodules or papules with a “rolled edge” forming around a central depression that may or may not be ulcerated, crusted and bleeding

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45
Q

Superficial BCC

A

Dry. scaly lesions, superficial flat growths may be misdiagnosed as eczema or psoriasis. Edge shows a “threadlike” raised b border

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46
Q

Morpheaform (sclerosing) BCC

A

Appear as a white sclerotic plaque w/ telangiectasia, scar-like in appearance

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47
Q

Pigmented BCC

A

Similar to nodular but brown or black pigmentation is present. Mostly found in dark skinned people

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48
Q

How can we diagnose BCC?

A

Biopsy; consists of large, round or oval tumor island within the dermis w/ and epidermal attachment

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49
Q

Tx for BCC

A

Permanently cure with best cosmetic result, surgical topical and radiation options

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50
Q

What are the topical txs for BCC?

A

5% imiquimod for non-facial superficial BCCs less than 2cm in diameter
5-FU for superficial BCC

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51
Q

What is a surgical option for a BCC?

A

E&C Electrodessication and Currettage, cryotherapy, excision with margins, and Mohs micrographic surgery

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52
Q

How can E&C be discribed?

A

For superficial lesions, use sharp curette to scape away friable tumor until normal dermis is felt. Then area is electrodessicated to cause necrosis of cells

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53
Q

When would cryotherapy be a good option for BCC?

A

For pts who are debilitated with medical conditions that preclude other types of surgery, generally not recommended

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54
Q

Excision with margins for BCC

A

Has a high cure rate 95%, less effective in treating recurrent BCC, better for primary lesions

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55
Q

What is the gold standard treatment for BCC?

A

Mohs Micrographic surgery

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56
Q

Mohs micrographic surgery

A

If tumor is >2cm and on facial area. Take small layer at a time and examined under microscope, gives smallest defect ensuring the best cosmetic potential

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57
Q

When would radiation be used for pts with BCC?

A

Older pts who are not candidates for surgery or where surgical excision will be disfiguring. Takes 5-25 visits, cure rate can be 80-95%

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58
Q

What is the prognosis for a pt with BCC?

A

Good is appropriate method of tx is used. Recurrent cancers are harder to cure. 100% survival if it hasn’t metastasized.

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59
Q

What type of cancer can arise from the malignant proliferation of epidermal keratinocytes?

A

Squamous cell carcinoma

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60
Q

What can put you at risk for SCC?

A

> 50yrs, light skinned males, tobacco/alcohol use, nonmelanoma skin cancer, HPV, immunosuppression, chemical carcinogens

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61
Q

What is characterized by the irregular nest of epidermal cells invading the dermis to varying degrees?

A

SCC

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62
Q

What are the two types of SCC?

A

SCC in situ (Bowen’s Disease) or invasive

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63
Q

Which layers does Bowen’s disease of SCC effect

A

Full thickness of epidermis

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64
Q

Which layers does invasive SCC effect

A

Penetrates into the dermis

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65
Q

Clinical manifestations of SCC

A

Begins at AK site, can be superficial papules, plaques, or nodules discrete and hard arising from indurated, round elevated base

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66
Q

Lower lip SCC

A

Starts as actinic chelitis, local thickening then a firm nodule, then can grow out as a sizeable tumor. Usually with hx of smoking

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67
Q

Periungual SCC

A

Presents with swelling, erythema and localized pain. Commonly in nail folds of hands resembling a wart

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68
Q

What is the histologic hallmark of SCC?

A

Presence of keratin of “keratin pearls” (well formed desmosome attachments and intracytoplasmic bundles of keratin)

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69
Q

Dx of SCC

A

Biopsy to find keratin pearls, lymphadenopathy on palpation in adjacent lymph nodes

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70
Q

What are the 3 treatment options for SCC?

A

Excision, Mohs, radiation

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71
Q

What is the prognosis of SCC?

A

Mohs 94-99%, metastasis associated with poor prognosis

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72
Q

Which pts have a better prognosis for SCC?

A

Pts w/ in-transit or regional metastasis as 1st site have better chance than those whose initial diagnosis included a distant nodal site

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73
Q

How often must pts with SCC come for follow ups?

A

Annual skin check every year

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74
Q

What is skin cancer of the melanocyte?

A

Melanoma

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75
Q

What does MMRISK stand for?

A 
Moles: atypical
Moles >50 common molves
Red hair and freckles
Inability to tan
Sunburn
Kindred/family history
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76
Q

Etiology of melanoma

A

Damage to DNA of melanocyte, non-inherited BRAF oncogene mutation, CDKN2A and CDK4 mutated tumor suppressor genes

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77
Q

Where does melanoma originate?

A

From melanocytes via the dermoepidermal junction

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78
Q

What is the greatest risk factor for metastasis?

A

Depth of the invasion

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79
Q

Clinical manifestations of melanoma

A

Macular, nodular, color varies from white non-pigmented to dark black blue or red. Lesions borders tend to be irregular, growth is quick or slow, distribution can be non sun exposed areas

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80
Q

ABCD of melanoma

A

Asymmetry, border (irregular), color (varied), diameter (>6mm)

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81
Q

Which type of melanoma does not have a preference for sun damaged skin?

A

Superficial spreading

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82
Q

Superficial spreading melanoma

A

Tendency to multicoloration including black, red, brown, blue, and white. Borders more sharply defined

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83
Q

Which type of melanoma starts as macular and flat then becomes nodular?

A

Lentigo Maligna

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84
Q

Which type of melanoma has an insidious slow growth?

A

Lentigo Maligna

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85
Q

Nodular Melanoma

A

Arise w/out radial growth phase, head neck and trunk, smooth and dome shaped, friable or ulcerated and bleeding

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86
Q

Which type of melanoma is common in darker skin types?

A

Acral-Lentiginous

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87
Q

Acral-Lentiginous melanoma

A

Light brown uniform pigmentation initially, on palms, soles, or nail beds. Lesion becomes darker, nodular and may ulcerate

88
Q

Which type of melanoma typically has a delay in diagnosis?

A

Acral-Lentiginous

89
Q

What can be the first sign of metastasis in melanoma?

A

Early mets occurring in lymphatics and regional lymphadenopathy

90
Q

Melanoma metastasis

A

Lymphatics first, then satellite metastases appear as pigmented nodules, then spreads via blood stream to any site including skin, brain, lung, and bone

91
Q

How is melanoma staged?

A

T (tumor) N (lymph node) M (metastasis)

92
Q

What is the T stage for?

A

How far the tumor has grown in the skin. Assigned 0-4 based on the depth

93
Q

What is the N stage for?

A

Assigned 0-3 based on whether it has spread to lymph nodes or lymph channels

94
Q

What is the M stage for?

A

Based on which organs and blood levels of LDH

95
Q

T1

A

Tumor 1.0mm or less

96
Q

T2

A

1.01mm-2.0mm

97
Q

T3

A

2.01mm04.0mm

98
Q

T4

A

> 4.0mm

99
Q

N1

A

One lymph node involved

100
Q

N2

A

Two or three lymph nodes involved

101
Q

N3

A

Four or more lymph nodes involved

102
Q

M0

A

No detectable evidence of distant metastases

103
Q

M1a

A

Metastases to skin, subQ, or distant lymph node, NORMAL SERUM LDH

104
Q

M1b

A

Lung metastases, NORMAL LDH

105
Q

M1c

A

Elevated LDH

106
Q

What is Breslow thickness?

A

The total vertical height of melanoma, from very top granular layer to area of deepest penetration.

107
Q

Less than 1mm Breslow thickness

A

5-yr survival is 95-100%

108
Q

1-2mm Breslow thickness?

A

5-yr survival is 80-96%

109
Q

2.1-4mm Breslow thickness?

A

5-yr survival is 60-75%

110
Q

> 4mm Breslow thickness?

A

5-yr survival 37-50%

111
Q

Melanoma Dx

A

Excisional biopsy preferred, take entire lesion out to see how deep it goes. Palpate lymph glands as well!

112
Q

Melanoma workup

A

LDH can be prognostic, 3A: CXR, 3B/C: fine needle aspiration of lymphs, 4: Abdominal or pelvic imaging or PET scan

113
Q

What is the surgical tx for melanoma?

A

Simple excision for early stage. For primary: wide local excision with sentinel lymph node biopsy or dissection

114
Q

When can radiation be given for melanoma pts?

A

As an adjuvant to surgery in area where lymph nodes were removed, used to relieve symptoms caused by metastases to brain or bone

115
Q

When is chemotherapy used for melanoma?

A

Advanced cases, to relieve symptoms and extend survival. Given in cycles lasting a few weeks

116
Q

What are some adjunct therapies for melanoma?

A

Cytokines (interferon-alpha and IL-2) which can help shrink advanced melanomas, can also be used with chemo drugs

117
Q

What is Vemurafenib used for?

A

Inhibits growth of melanoma w/ some mutated forms of BRAF for late stage melanoma

118
Q

What is Dabrafenib used for?

A

BRAF inhibitor for an unresectable or metastatic melanoma

119
Q

What is Trametinib used for?

A

MEK inhibitor for an unresectable or metastatic melanoma

120
Q

Follow up for pts w/ melanoma

A

Every 6 mos full skin check, self skin checks 1/mo and sun protection

121
Q

Which virus spreads via respiratory droplets and has an incubation period of 9-12 days?

A

Measles (Rubeola)

122
Q

How long does it take for measles to clear?

A

4-7 days

123
Q

Si/Sx of measles

A

Prodrome of cough, coryza, conjunctivitis, fever, then rash develops

124
Q

What do the measles lesions look like?

A

Start as macular or morbilliform rash on anterior scalp and behind ears then by day 2 or 3 down the trunk to the extremities

125
Q

What are Koplick spots?

A

Pathognomonic white papules 1mm on buccal mucosa and pharynx (measles)

126
Q

Do the lesions for measles spread to the palms and soles?

A

Yes

127
Q

What is the treatment of measles?

A

Vaccination w/live virus at 15 mo and 5 yrs, and supportive therapy (rest, fluids, etc.)

128
Q

What is caused by the Toga virus?

A

Rubella, German Measles

129
Q

How are the german measles spread?

A

Respiratory secretions, 12-23 incubation period

130
Q

Si/Sx of German Measles

A

Pain with LATERAL UPWARD EYE MOVEMENT, lymphadenopathy, begins on face and spreads inferior covering body in 24h

131
Q

What is Forsceimer’s sign?

A

Pitechiae on soft palate and uvula (German Measles)

132
Q

What do the lesions look like in Rubella?

A

Pale pink morbilliform macules smaller than rubeola

133
Q

What is the treatment for German Measles?

A

Vaccination with MMR, supportive therapy

134
Q

A benign infectious exanthem caused by Parovirus

A

Fifth Disease (Erythema Infectiosum)

135
Q

How is 5th disease spread?

A

Respiratory droplets

136
Q

Erythema Infectiosum

A

Viral shedding stops by the time symptoms appear (when no longer infectious), incubation of 4-14 days

137
Q

What are the 3 phases of Erythema Infectiosum?

A
  1. Abrupt erythema of cheeks (slapped cheek)
  2. Day 4-erythematous macules on proximal extremities and trunk evolving into lacy pattern by day 9
  3. Recurring stage with heat or sunlight
138
Q

Treatment for 5th disease?

A

Supportive therapy

139
Q

What is Pityriasis Rosea?

A

An acute benign self-limiting eruption common in spring/fall w/unknown cause

140
Q

Herald Patch

A

2-5cm scaly lesion that may mimic tinea corporis (Pityriasis Rosea)

141
Q

Si/Sx for Pityriasis Rosea

A

Over 2 weeks oval or elliptic erythematous patches w/fine scale. “Christmas tree” like pattern on trunk. Viral symptoms may occur

142
Q

What do the lesions look like in Pityriasis Rosea?

A

Macular or papular lesions develop on trunk, neck, extremities. May be pruritic

143
Q

How long does Pityriasis Rosea last?

A

3-8 weeks, resolves spontaneously

144
Q

How can you treat Pityriasis Rosea?

A

Not needed, antihistamines for pruritis

145
Q

The most common form of adverse drug eruptions

A

Morbilliform reactions

146
Q

What is the patho behind morbilliform rxns?

A

Type 4 allergic rxn mediated by T-helper cells

147
Q

Morbilliform rxns commonly caused by which drugs?

A

Ampicillin, amoxicillin, bactrim

148
Q

Si/Sx of a morbilliform rxn

A

Erythema w/macules and papules intitally on trunk then generalizing w/in 2 days.

149
Q

How long can the si/sx last for a morbilliform reaction?

A

Can present within first 2 weeks of exposure up to 10 days after

150
Q

Treatment for morbilliform reaction?

A

Clears within 2 weeks of stopping medication, can use antihistamines and low potency topical steroids

151
Q

A fixed drug reaction happens when?

A

Usually with meds taken intermittently, NSAIDs, Sulfonamides, Barbiturates

152
Q

What do the lesions look like in a fixed drug reaction?

A

Round/oval erythematous plaques may be pruritic/burning or asymptomatic. Usually 6 or few lesions, usually 1

153
Q

Where do the lesions appear in a fixed drug reaction?

A

Genitals or oral mucosa

154
Q

What is the treatment for a fixed drug reaction?

A

Stop drug, if symptomatic can use antihistamines or topical steroid

155
Q

What is a self-limited eruption brought on by drug exposure viral infections or can be idiopathic?

A

Erythema Multiforme

156
Q

What drugs can cause erythema multiforme?

A

Sulfa, Barbs, PCN, Phenytoin

157
Q

What do the lesions look like in erythema multiforme?

A

Begin as macules and become papular then vesicles and bullae form in the center of papules. Localized to hands and feet

158
Q

Si/sx of erythema multiforme

A

Mucosal lesions are painful and erode, fever, malaise

159
Q

Treatment of erythema multiforme?

A

Avoid target substances, sever reaction may require systemic steroids

160
Q

SJS and TEN

A

Mucocutaneous blistering rxn from drug rxn

161
Q

SJS is thought to be a severe variant of what?

A

Erythema Multiforme

162
Q

TEN is thought so be a severe variant of what?

A

SJS

163
Q

Si/Sx of SJS and TEN

A

Fever, mucosal inflammation. Lesions begin on trunk and may be painful, TEN exhibits higher fever and more epidermal separation then SJS

164
Q

Tx of SJS and TEN

A

Withdrawal of offending agent, treatment at burn center for fluid and electrolyte imbalance, wound care

165
Q

What is Bullous pemphigoid?

A

Autoimmune presents in 6th decade of life caused by autoantibodies, complement fixation, neutrophil and eosinophils

166
Q

What type of antibodies bind to basement membrane in bullous pemphigoid?

A

IgG antibodies

167
Q

What do the IgG antibodies activate?

A

Activates complement and inflammatory mediators, attracting cells to basement membrane and releasing proteases

168
Q

Proteases lead to what?

A

Blister formation (Bullous Pemphigoid)

169
Q

The blister is formed how?

A

By cleavage of the basal cells away from the basal lamina

170
Q

What are the lesions like in bullous pemphigoid?

A

Bullae are large and may contain serous or hemorrhagic fluid. Targets the axillae, thighs, groin and abdomen

171
Q

What is the course and prognosis of bullous pemphigoid?

A

Usually self-limiting over a 5-6 year period

172
Q

How can you diagnose bullous pemphigoid?

A

Biopsy and immunofluorescence. C3 deposition is nearly always present in BP

173
Q

Tx for localized or limited bullous pemphigoid

A

Potent topical steroid, Clobetasol with occlusion

174
Q

Tx for moderate and severe bullous pemphigoid

A

Prednisone, once in remission can taper cautiously

175
Q

What can be considered for pts that cant handle steroids? (bullous pemphigoid)

A

Immunosuppressive meds

176
Q

What other meds have been helpful with bullous pemphigoid?

A

Azathioprine, Mycophenolate mofetil, the combo of Tetracycline and Niacinamide, TCN, Doxy or Minocycline (instead of TCN), Dapsone, Recalcitrant

177
Q

What is pediculosis?

A

Lice

178
Q

How long does it take the eggs to hatch on hair shafts?

A

One week

179
Q

Pediculus humanus capitis

A

Scalp

180
Q

Pediculus humanus corporis

A

Body

181
Q

Phthirus pubis

A

Pubic area (crabs)

182
Q

The female louse cannot survive for more than _ days off the human head

A

3

183
Q

Where does the body louse live?

A

Not on the human body, lives in human clothing crawling onto the body only to feed at night

184
Q

The adult female body louse can survive how long away from human body?

A

10 days

185
Q

P.pubis are different from head and body louse how?

A

Shorter, broader body with large front claws, making it able to grasp the coarser pubic hairs

186
Q

Heavy infestation of crabs can also involve where?

A

Eyelashes, eyebrows, facial hair, and the periphery of the scalp

187
Q

How long can the pubic louse survive away from human body?

A

1 day

188
Q

Si/sx of pediculosis capitus (head lice)

A

Present w/intense pruritus of scalp with posterior cervical lymphadenopathy, excoriations and small specks of louse dung on scalp

189
Q

Si/sx of pediculosis corporis (body lice)

A

Initially small pruritic papules that progress to scratching, crusted and infected papules, Spares the hands and feet

190
Q

Si/sx of pediculosis pubis (crabs)

A

Intense pruritis in affected areas, small blue macules can present

191
Q

Dx of pediculosis

A

History, microscopic examination, biopsy

192
Q

What are some topical treatment options for pediculosis?

A

OTC Nix cream Rinse, RID Acticin

193
Q

What is the active ingredient in Nix cream rinse and RID Acticin

A

Permethrin. Acts as neurotoxin and paralysis of nerves in parasite leading to death

194
Q

When should you repeat treatment?

A

One week later. Permethrin only kills active louse, not the nits.

195
Q

Ovid lotion

A

Topical treatment for pediculosis. Most effective for head louse. NOT FOR CHILDREN <6mos. Apply to dry hair let sit for 8-12 hours

196
Q

Elimite cream

A

Has 5% permetherin, leave on overnight and repeat in one week

197
Q

What else can be used to treat pediculosis?

A

Bactrim and vasaline. *Treat entire family**

198
Q

What is environment eradication?

A

Fomites should be washed in hot water and dried. Should be exposed to temps >50-55C for atleast 5 mins to kill any bugs left. Can also seal in a plastic bag for 2 days

199
Q

What is an infestation w. the Sarcoptes scabiei

A

Scabies

200
Q

Mites burrow into epidermis and deposit feces and lay eggs in what?

A

Scabies

201
Q

What type of reaction happens with scabies?

A

Type 4 hypersensitivity reaction about 30 days after infestation

202
Q

Scabies should be considered when?

A

Any patient with persistent pruritis not responding to topical steroids

203
Q

Si/sx of scabies

A

Pruritic lesion vary from vesicles or papule, nodules located b/w web space of finers, flexor aspects of wrists, axilla, antecubital area, abdomen, umbilicus, genital gluteal areas, and feet

204
Q

Where does scabies spare on the body?

A

Face

205
Q

Burrow

A

Pathognomonic of scabies infestation, appearing as a thin short gray brown, wavy channel on the skin

206
Q

Crusted/Norwegian scabies

A

Immunocompromised or debilitated pts. Crusts and scales teem with mites. Psoriasis like scaling around nails with crusting

207
Q

Topical treatment for scabies

A

Permethrin, apply to skin for 8 hrs
Lindane not for pregnant or kids
Percipitated Sulfar best for pregnant pts, all for 8-10 hrs

208
Q

Oral treatment for scabies

A

Ivermectin

After treatment: bedding, clothing, towels washed in hot water or removed for 72 hrs

209
Q

Loxoscelism is what?

A

Brown recluse spider bite

210
Q

How is the brown recluse spider identified?

A

Dark, violin-shaped markings over cephalothorax and 3 sets of eyes rather than usual 4

211
Q

What does the brown recluse spiders venom contain?

A

Phospholipase enzyme, sphingomyelinase D which is a major toxin

212
Q

Si/sx of brown recluse spider bite

A

Bite site painful after 3 hrs, necrotic cutaneous loxoscelism, extensive necrosis develops with edema w/in 8hrs with bulla and surrounding erythema and ischemia that can extend to muscles

213
Q

Treatment for brown recluse spider bite

A

Rest, ice and elevation of site, analgesics, tetanus prophylaxis and surgical debridement

214
Q

Si/sx of black widow spider (lactrodectism) bite

A

Locally limited to small circle of redness. Systemically: pain/cramping within an hour, tachycardia, HTN, PE, fevers, chills, vomiting, violent cramps, delirium or partial paralysis

215
Q

Treatment of black widow spider bite

A

ACLS, antivenom administer in ER, analgesics (Morphine), antihistamine (Benadryl), tetanus

Clin med 1 (9 decks)

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