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Dermatology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

THis is a collection of pus (neutrophils) that has accumulated within a tissue because of an inflammatory process.

A

Abscess

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2
Q

This is an infection of the hair follicle, which may progress to cutaneous tissue, leading to furuncles (boils).

A

Folliculitis

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3
Q

These are large, painful, raised nodules that contain underlying collections of dead and necrotic cells in cutaneous tissues.

A

Furuncles (boils)

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4
Q

These are an extension of furuncles into subQ tissues.

A

Carbuncles

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5
Q

This is a spreading infection that is limited tot he epidermis and presents as a bullous, crusted, or pustular eruption of the skin.

A

Impetigo

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6
Q

What characteristic color are the lesions in impetigo?

A

Honey-crusted lesions

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7
Q

This is a spreading infection that involves the blocking of dermal lymphatics and presents as a well-defined, spreading erythematous inflammaton, and often accompanied by pain and fever.

A

Erysipelas

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8
Q

In which age does a malar (butterfly) bright red rash occur on the face as an erysipelas?

A

Children

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9
Q

This is a spreading infection where the focus of the infection is in the subQ fat.

A

Cellulitis

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10
Q

This is the inflammatory response to infection of the soft tissue below the dermis, rapid spread along the fascial planes, disrupting the blood suppy.

A

Necrotizing fasciitis

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11
Q

Ischemia of the muscle layer can cause this condition, where there is gas resulting from the fermentative metabolism of anaerobic organisms.

A

Gas Gangene

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12
Q

This is a flat red local inflammation in response to an infiltrating leukocyte (esp their toxins in the dermis).

A

Macule

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13
Q

This is a raised red inflammation with invasion of neighboring tissues.

A

Papule

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14
Q

This is a small blister, from a microbe that invades the epithelium (HSV, VZV).

A

Vesicle

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15
Q

This is the ruptured epithelium from a vesicle, where the microbe is discharged.

A

Ulder

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16
Q

This is when the microbe grows into the epitheliu, which proliferates, and the microbe sheds with epithelial cells (wart).

A

Papilloma

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17
Q

What is the most common cause of skin infections?

A

S. aureus

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18
Q

What are the lab chracteristics of S. aureus?

A

G+ cocci
Catalase +
Coag +
B-hemolytic

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19
Q

After S. aureus invasion to the skin, what forms within 2-4 days?

A

Boil

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20
Q

After the boil in the S. aureus forms, it triggers an inflammatory response and the invasion of Neutrophils to cause what to form?

A

Abscess

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21
Q

What happens to the abscess in S. aureus infections?

A

Expands and eventually drains.

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22
Q

What is the DOC for bacteria that produce B-lactamase?

A

Methcillin

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23
Q

What is the DOC for MSSA?

A

Nafcillin

susceptible

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24
Q

What is the DOC for MRSA?

A

Vancomycin

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25
Q

Nasal carries of MRSA can be treated with nasal creams, like what drug?

A

Mupirocin

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26
Q

What does MRSA secrete, which has a lower affinity for B-lactams than normal PBPs, allowing it to continue cell wall synthesis when other PBPs are inhibited.?

A

PBP2a

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27
Q

What gene codes for PBP2a?

A

MecA

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28
Q

Vancomycin resistance comes from a ligase producing pentapeptides terminating in what sequence?

A

D-Ala D-lactate

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29
Q

Which Van genes can be transmitted (chromosomal or plasmid) and inducible?

A

VanA and VanB can be transmitted and is inducible.

VanD cannot be transmitted (chromosomal) and expressed constitutively

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30
Q

True or False: S. aureus have decreased susceptibility to vancomycin from Van genes.

A

False

Decreases susceptibility is associated with cell wall composition (↑ thickness) and not a Van gene.

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31
Q

Which Van comes from VRE from a plasmid and has high-level glycopeptide resistance?

A

VanA gene

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32
Q

Which toxin causes SSSS?

A

Exfoliatin or SSS toxin

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33
Q

Which ages is SSSS common?

A

Neonates

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34
Q

What is the manifestations of SSSS?

A

Large blisters with clear fluid and skin loss, mimics burns.

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35
Q

What is the mechanism of action of the TSST1 to cause TSS?

A

Superantigen (overstimulation of T cells and macrophages)

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36
Q

What “device” causes young girls to be susceptible to TSS?

A

Tampons

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37
Q

What are the Sx to TSS?

A

Fever, hypoTN, diffuse macular erythematous rash followed by desquamation of the skin (esp soles/palms)

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38
Q

What is the main virulence factor for S. pyogenes?

A

M protein

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39
Q

How does M protein provide resistance from S. pyogenes infections?

A

Inhibition of opsonization

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40
Q

After 1-2 days, there is an inflammatory response made from S. pyogenes infections, and it spreads using what protein?

A

Hyaluronidase

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41
Q

What are the superantigens called in S. pyogenes?

A

SPE’s (A, B, and C)

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42
Q

This is the superficial infection of S. pyogenes.

A

Impetigo

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43
Q

What is the deeper infection of the dermis called in S. pyogenes, where there can be bacteriemia and death?

A

Erysipelas

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44
Q

What is the condition from S. pyogenes where there is immune complex deposition on the BM of the glomerulus 2-3 weeks after infection?

A

PSGN

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45
Q

What is teh condition from S. pyogenes infection that is a mixed infection of anaerobes and faculative anerobes, and there is widespread necrosis of the skin and possible death?

A

Necrotizing fasciitis

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46
Q

What are the 2 main suspects to Cellulitis?

A

S. pyogenes

S. aureus

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47
Q

Which bacteria is G+, cocci, catalase -, B hemolytic, bactitracin sensitive, PYR+, and ASO+?

A

S. pyogenes

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48
Q

What is the source for S. pyogenes cellulitis?

A

Normal flora –> trauma causes inoculation

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49
Q

Which bacteria is G+, cocci, catalase +, coag +, and mannitol fermenting?

A

S. aureus

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50
Q

Which VF from S. aureus binds the Fc portion of host IgG?

A

Protein A

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51
Q

What cause of cellulitis is a G+ rod, catalase-, non-spore forming, and nonmotile?

A

Erysipelothrix rhusiopathiae

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52
Q

What is the host for Erysipelothrix rhusiopathiae infections?

A

Pigs

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53
Q

What is the cause of cellulitis that is G- rod, comma shaped, lactose non-fermenter, oxidase +, and motile?

A

Vibrio vulnificus

Vibrio algionlyticus

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54
Q

Where can u get vibrio?

A

Marine invironments

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55
Q

Which bug can cause gas gangrene from the soil and feces?

A

C. perfringens

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56
Q

What does the Lecithinase (alpha toxin) cleave on the host cell membranes, leading to cell lysis and death?

A

Phospholipids

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57
Q

What are the 2 risk factors for gas gangrene?

A

Ischemic vascular disease

Peripheral arteriosclerosis

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58
Q

Which specialized agar differentiates C. perfrinegens from other bacteria?

A

+ Nagler rxn (egg yolk agar)

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59
Q

These are greasy plugs of keratin, sebum, and bacteria, capped by a layer of melanin.

A

Comedones (black heads)

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60
Q

What is the main cause of comedones, which an aerotolerant anaerobic G+ rod?

A

Proprionibacterium acnes

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61
Q

What hormones ↑ in the body to ↑ sebum and keratinization/desquamation in pilosebaceous ducts to cause acne/comedones?

A

Androgenic H’s

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62
Q

These are acid fast rods that stain with Ziehl-Neelsen or auramine stain.

A

M. leprae

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63
Q

Which 2 cells does M. leprae grow in?

A

Skin histiocytes

Schwann cells

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64
Q

True or False: like TB, M. leprae can be grown in vitro.

A

FALSE

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65
Q

Where can u find M. leprae in infected individuals?

A

Nasal secretions

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66
Q

How long is the incubation period for M. leprae?

A

Years

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67
Q

This is the form of leprosy where there is a vegrous CMI response, leading to phagocytic destruction of bacteria and exaggerated allergic response.

A

Tuberculoid leprosy

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68
Q

What is a common Sx of Tuberculoid leprosy?

A

Local anethesia from thickening of peripheal nerves

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69
Q

What is the CMI response to M. leprae to cause Lepromatous leprosy?

A

Weak CMI response

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70
Q

Which is worse, Lepromatous leprosy or Tuberculoid?

A

Lepromatous leprosy

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71
Q

What are the Sx to Lepromatous leprosy?

A

Loss of eyebrows
Thickening and enlargement of nostrils, ears, and cheeks
Lion-like face
Lose nasal septum

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72
Q

Which form of Leprosy (L or T) will have numerous organisms on staining?

A

Lepromatous leprosy

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73
Q

Which mycobacterium do u associate with fish tanks?

A

M. marinum

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74
Q

What usually happens to you to allow M. marinum into your skin?

A

Some sort of trauma

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75
Q

What is the initial lesion of M. marinum after 2-8 weeks?

A

Small papules –> enlarge and may ulcerate.

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76
Q

What are Mycobacterium genus that causes chronic, relatively painless cutaneous “buruli” ulcers?

A

M. ulcerans

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77
Q

Where can u find M. ulcerans?

A

Africa and Australia

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78
Q

Which form of fungi (yeast or mold) are unicellular, reproduce by budding, and can form pseudohyphae?

A

Yeast

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79
Q

So we can guess that molds are multicellular and have hyphae, but what are hyphae?

A

Elongated tubes of cells attached end to end

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80
Q

What are the form of hyphae that have membranes separating individual cells?

A

Septate hyphae

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81
Q

What are the 4 dimorphic fungi?

A

C. immitis
H. capsulatum
B. dermatidis
S. schenkii

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82
Q

Tinea pedis and vaginal candidiasis are of what type of mycoses infection?

A

Superficial

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83
Q

What is involved in subcutaneous mycoses?

A

Nails and deeper layers of the skin

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84
Q

What is it called when there are mycoses of the internal organs?

A

Systemic/Deep mycoses

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85
Q

Malassezia furfur- conditions

A

Pityriasis or Tinea versicolor

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86
Q

Malassezia furfur- lesion morphology

A

Hypo or Hyperpigmented macules that coalesce to form scaling plaques.

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87
Q

Malassezia furfur- Sx

A

Itchy lesions, resolve spontaneously

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88
Q

Malassezia furfur- findings on KOH prep

A

Spaghetti and meatballs

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89
Q

Malassezia furfur- Tx

A

Miconazole, selenium sulfide

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90
Q

This is is a common label for a group of 3 types of fungus that common causes skin disease in animals and humans.

A

Dermatophytes

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91
Q

What contacts the skin to cause dermatophytes?

A

Anthospores

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92
Q

What are the most common cause of dermatophyte infections, where the anthrospores are spread shed from human skin scales and hair?

A

Antropohphilic

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93
Q

What is the most common dermatophyte from animals?

A

Zoophilic

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94
Q

Where do the following Zoophilic dermatophytes come from?

Trichophyton verrucosum
T. mentagrophytes
Microsporum canis

A

Trichophyton verrucosum- cows
T. mentagrophytes- rodents
Microsporum canis- dogs and cats

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95
Q

What are the type of dermatophytes from soil, and includes species like Microsporum gypseum?

A

Geophilic

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96
Q

Which epidermal protein do the tinea spp like to infect?

A

Keratin (skin, hair, nails)

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97
Q

What is the typical lesion morphology in tinea infections?

A

Serpentine scaling patch with raised margin

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98
Q

Which tinea spp infects the hair and scalp, leading to hair loss?

A

Capitis

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99
Q

Which tinea spp infects the body?

A

Corporis

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100
Q

Which tinea spp infects the crotch?

A

Cruris

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101
Q

Which tinea spp infects the feet?

A

Manuum and Pedis

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102
Q

Which tinea spp infects the nails?

A

Unguium

these names are freakin weird

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103
Q

What are the 3 genera responsible for dermatophytoses?

A

Microsporum
Epidermophyton
Trichophyton

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104
Q

What type of “light” do you use to see the microsporum spp?

A

UV-emitting Wood’s light

105
Q

Using a UV-emitting Wood’s light, what color do the hairs flouresce if they are contaminated with microsporum spp?

A

Bright green

106
Q

If you have a bright red rash in a skin fold because youre 500 pounds and you need an innocent EMT working in the ICU to help cleanse your cheesy smelly skin folds, what fungi is prolly growing there?

A

Candida

107
Q

Which WBC are important for the prevention of superficial candida infections?

A

T-cells

108
Q

Which WBC are important for the prevention for hematogenous spread of candida?

A

Neutrophils

109
Q

If you get pricked by a rose bush and develop a small papule that subsequently spreads to the lymphatics, what fungi might be the cause?

A

Sporothrix schenckii

110
Q

What agar is used to Dx Sporothrix schenckii?

A

Sabouraud dextrose agar

111
Q

Which 3 viruses do not spread systemically?

A

Papillomas
Molluscum contagiosum
Orf

112
Q

What is the type of lesion of HSV, VZV, CoxA, and CoxB?

A

Vesicular

113
Q

A vesicular lesion shows a icosahedral, non-enveloped, dsDNA virus. What is the cause?

A

Papillomavirus

114
Q

Which HPV types cause plantar warts?

A

1 and 4

115
Q

Which HPV types cause genital warts?

A

6, 11

116
Q

Which HPV types cause warts on the knees and fingers?

A

2, 3, 10

117
Q

Papillomavirus- transmission

A

Direct contact

118
Q

Papillomavirus- layer of skin infected

A

Basal layer

119
Q

Papillomavirus- cancer associations

A

Cervical
Vulva
Penis
Rectum

120
Q

Molluscum contagiosum- genus

A

poxvirus

121
Q

Molluscum contagiosum- lesion morphology

A

Fleshy, umbilicated

122
Q

Molluscum contagiosum- transmission

A

Contact

123
Q

Orf- host

A

Sheep

124
Q

Orf- lesion morphology

A

Papulovesicular, generally on hands, may ulcerate

125
Q

What type of host envelope do the herpesviridae acquire?

A

Nuclear membrane envelope

126
Q

What type of cells are seen on Tzanck smear for herpes?

A

Multinucleated Giant cells

127
Q

What “bodies” are seen in herpes?

A

Eosinophilic Cowdry intranuclear inclusion bodies

128
Q

HSV1- diseases

A

Gingivostomatitis, keratoconjunctivitis, herpes, ENCEPHALITIS

129
Q

HSV1- transmission

A

Kiss kiss

130
Q

HSV1- location for focal necrotic lesions

A

Temporal lobe

131
Q

HSV1- site of latency

A

Trigeminal gangkion

132
Q

HSV1- triggers

A

stress

133
Q

HSV2- diseases

A

genital herpes, neonatal herpes

134
Q

HSV2- transmission

A

sexual contact

135
Q

HSV2- Sx

A

local vesicular lesions

136
Q

HSV2- group at complication risk

A

Pregnant ladies

137
Q

HSV2- site of latency

A

Sacral ganglia

138
Q

HSV2- trigger

A

Stress

139
Q

VZV- diseases

A

varicella (chickenpox) and zoster (shingles)

140
Q

VZV- transmission

A

Respiratory secretions

141
Q

VZV- morphology of vesicles in respiratory tract

A

Dew on a rose petal

142
Q

VZV- primary presentation

A

Rash with vescicles (varicella), resolves in 2 weeks

143
Q

VZV- secondary presentation

A

Shingles, painful vesicular rash over 1 dermatome

144
Q

VZV- 3 complications

A

Interstitial PNA
CNS involvement
Blindness

145
Q

VZV- site of latency

A

DRG

146
Q

VZV- triggers

A

Stress, IC state, ↑ age, local injury

147
Q

Which viral family does coxsackie virus A16 belong to?

A

Picornaviruses

148
Q

Coxsackie A16- viral characteristics

A

ss + linear RNA, nonenveloped, iscosahedral

149
Q

Coxsackie A16- 2 diseases

A

Herpangina (mouth blisters, fever)

Hand, Foot, Mouth disease

150
Q

Coxsackie A16- transmission

A

Fecal oral or direct contact or aersolization

151
Q

Parvovirus B19- genome morphology

A

ssDNA

152
Q

Parvovirus B19- 2 diseases

A 
Erythema Infectiosum (5th disease)
Aplastic anemia crisis
153
Q

Parvovirus B19- 5th disease Sx

A

Cheek rash (slapped cheeks) –> move down to trunk

154
Q

Parvovirus B19- transmission

A

Respiratory aerosols

155
Q

Parvovirus B19- vertical transmission conditions

A

Fetal anemia

Hydrops fetalis

156
Q

HHV6- disease

A

Roselia

157
Q

HHV6- Sx

A

Fever followed by a lacy body rash within 2 days

possible szrs

158
Q

HHV6- transmission

A

Saliva

159
Q

HHV7- disease

A

Roselia (though not as frequently)

160
Q

HHV8- disease

A

Kaposi sarcoma

161
Q

HHV8- pts at risk

A

AIDS

162
Q

HHV8- lesion morphology

A

Nodular and dark (purplish)

163
Q

HHV8- transmission

A

Secks

164
Q

Poxvirus- morphology

A

Complex (not enveloped)

165
Q

Poxvirus- site of replication

A

Cytoplasm (not in nucleus, despite being a DNA virus)

166
Q

Since poxvirus replicates in the cytoplasm, what enzyme must it contain to replicate within the cytoplasm?

A

DNA-dependent RNA polymerase

167
Q

Poxvirus- transmission

A

Person-person with skin lesions and via respiratory tract

168
Q

Poxvirus- disease

A

Smallpox

169
Q

Poxvirus- lesion morphology

A

Vasiculopapular rash with later scarring, especially on the face

170
Q

Poxvirus- vaccine type

A

Live attenuated

171
Q

What was it about the following things that made it possible for smallpox to be eradicated?

Subclinical features
Carriers
Host
Vaccine

A

No subclinical features
No carriers
Humans were the only host
Effective vaccine was available.

172
Q

What was the most recent scare in the US related to smallpox due to?

A

Monkeypox

173
Q

What was the carrier for monkeypox to infect 80 people in the US?

A

Prairie dogs

174
Q

Measles- virus morphology

A

dsDNA, linear

175
Q

Measles- transmission

A

Respiratory droplets

176
Q

What was the name of the Arabian physician that first recognized measles over 1000 years ago?

A

Rhazes

177
Q

Measles- first Sx

A

Runny nose, fever, cough, conjunctivits

178
Q

Measles- lesion morphology

A

Koplik spots- white spots on buccal mucosa

179
Q

Measles- spread of rash

A

Starts on the face and then spreads down the trunk to the limbs

180
Q

Rubella- class of virus

A

Togavirus

181
Q

Rubella- viral characterisitics

A

+ ssRNA, linear, icosahedral, envelope with E1, E2 surface glycoproteins

182
Q

Rubella- transmission

A

Transplacental or Airborne

183
Q

After entering the respiratory tract, where does rubella enter?

A

Lymph nodes and spleen

184
Q

After multiplying in the lymph nodes, where does the virus then invade?

A 
Respiratory tract
Skin
Placenta
Joints
Kidneys
185
Q

What are the Sx of rubella invasion of the respiratory tract?

A

Sore throat, coryza, cough

186
Q

What are the Sx of rubella invasion of the skin?

A

rash from forehead –> down

187
Q

What are the Sx of rubella invasion of the placenta?

A

Congential rubella (PDA, cataracts, deafness, microcephaly)

188
Q

What are the Sx of rubella invasion of the joints?

A

RA

189
Q

R. rickettsi- disease

A

RMSF

190
Q

R. rickettsi- vector

A

Wood tick (dermacentor andersoni)

191
Q

R. rickettsi- spread of rash

A

palms/soles –> trunk

192
Q

R. rickettsi- complications

A

edema + hemorrhage –> hypovolemia

193
Q

R. rickettsi- area of infection in the US

A

North Carolina and Oaklahoma

194
Q

Borrelia burgdoferi- disease

A

Lyme disease

195
Q

Borrelia burgdoferi- vector

A

Ixodes tick

196
Q

Borrelia burgdoferi- stages

A
  1. erythema migrans
  2. neuropathy
  3. arthritis
197
Q

Borrelia burgdoferi- rash morphology

A

Bulls eye that expands

198
Q

Bacillus anthracis- disease

A

Anthrax

199
Q

Bacillus anthracis- population at risk

A

herbivores

200
Q

Bacillus anthracis- bacterium morphology

A

G+ rod (boxcar shaped)

201
Q

Bacillus anthracis- capsule morphology

A

D-glutamic acid

protein capsule. the only bacteria to have a protein capsule. super important

202
Q

Bacillus anthracis- toxins

A

PA
EF- ↑ cAMP
LF- protease

203
Q

Bacillus anthracis- skin manifestations

A

Painless ulcer with black eschar and edema called a malignant pustule

204
Q

Bacillus anthracis- pulmonary findings

A

If inhaled –> hemorrhagic mediastinitis (widened) –> septic shock and death

205
Q

Bacillus anthracis- GI findings

A

Ingestion of contaminated meats –> N/V, bloody diarrhea, death

206
Q

Bacillus anthracis- Tx

A

PCN

207
Q

Yersinia pestis- disease

A

Plague

208
Q

Yersinia pestis- vector

A

fleas

209
Q

Yersinia pestis- host

A

Rodents

210
Q

Yersinia pestis- VF

A

Capsule

211
Q

Yersinia pestis- morphology

A

non-motile, non-lactose fermenting, SAFETY PIN, growth at 4 degrees

212
Q

Yersinia pestis- plague Sx

A

High fever, buboes

No human-human

213
Q

Yersinia pestis- penumonic plague transmission

A

Human-human

214
Q

Pasteurella multocida- host

A

Cats and Dogs

215
Q

Pasteurella multocida- transmission

A

Cat/Dog bite

216
Q

Pasteurella multocida- Sx

A

Cellulitis

217
Q

Pasteurella multocida- lab characterisitics

A

G- rod, bipolar (safety pin) staining, capsule, musty odor

218
Q

Pasteurella multocida- agar

A

Chocolate or blood at 37 degrees

219
Q

Ancylostoma braziliense- appearance

A

Hookworm

220
Q

Ancylostoma braziliense- host

A

Dog and cat intestines

221
Q

Ancylostoma braziliense- people at risk

A

Kids who play with dog and cat poop

222
Q

Ancylostoma braziliense- distribution

A

Beaches throughout the US

223
Q

Ancylostoma braziliense- Sx

A

Severe erythematous and vesicular reactions

224
Q

Ancylostoma braziliense- syndrome at risk

A

Loffler syndrome- transient pulmonary infiltrate with peripheral eosinophilia

225
Q

Ancylostoma braziliense- Dx method

A

Skin biopsy shows larvae, Hx of playing with dog poop

226
Q

Ancylostoma braziliense- Tx

A

Albendazole

227
Q

Who deemed the name the “fiery serpent” to Dracunculus medinesis (aka the little dragon of Medina) with the Israelites at the Red Sea?

A

Moses

228
Q

Dacunculus medinesis- appearance

A

Tissue-invading nematode from the Cyclops genus

229
Q

Dacunculus medinesis- life cycle

A

larve ingested in drinking water –> penetrate GI wall –> maturation and mating in retroperitoneum –> subQ tissues –> ulcer –> larvae released once water contacts them.

230
Q

Dacunculus medinesis- risky behavior to get infected

A

Drinking from “step wells”

231
Q

Dacunculus medinesis- geographical distribution

A

Asia and Africa

232
Q

Dacunculus medinesis- time until ulcer appearance

A

1 year

233
Q

Dacunculus medinesis- Sx

A

Pain and erythema at the ulcer site

234
Q

Dacunculus medinesis- Dx method

A

Flood the ulcer with water and wait until the worms crawl out

235
Q

Dacunculus medinesis- Ancient method of Tx

A

Slowly wrapping the worm on a twig

236
Q

Dacunculus medinesis- New Tx method

A

Surgical removal

237
Q

Black widow (L. mactans)- distribution

A

Wood piles and brush in the South

238
Q

Black widow (L. mactans)- pathogenesis

A

Sharp pain at bite –> local swelling, reness, and burning –> systemic signs like boardlike abd, chest pain, N/V –> Sx subside within 48 hours

239
Q

Black widow (L. mactans)- toxin MOA

A

↑ presynaptic release of Ach

240
Q

Black widow (L. mactans)- Tx

A

Antivenin to kids/weak people

241
Q

Brown Recluse (Loxosceles)- pathogenesis

A

painless –> hours there is itching, swelling, and soreness and bleb at the site –> 3 days there is ulceration and radiating necrosis –> possible systemic problems.

242
Q

How long does it normally take to have Sx if you’ve never been bit by scabies?

A

weeks-months

243
Q

How long does it take to have Sx if you’ve been previously exposed?

A

1-4 days

244
Q

What type of HS rxn causes the sensitization to scabies?

A

Type IV

245
Q

Scabies- appearance

A

Oval, saclike body with claws

246
Q

Scabies- Epidemiology

A

Found everywhere

247
Q

Scabies- pathogenesis

A

Enter skin –> burrows under epidermis –> female lays eggs in skin burrows (esp folds) –> intense itching

248
Q

Scabies- Dx method

A

Skin scrapings

249
Q

Scabies- Tx

A

1% gamma benzene hexachloride (lindane)

5% permetrin cream (Enlimite) (this is better)

250
Q

Lice (P. humanus capitis)- appearance

A

Elongated, wingless, flattened insets with 3 legs and a pretty mouth.

251
Q

Lice (P. humanus capitis)- Epidemiology

A

KIDS

252
Q

Lice (P. humanus capitis)- Sx

A

Intense itching, possible pruritic red papules around the ears, face, neck, or shoulders.

253
Q

Lice (P. humanus capitis)- Dx

A

See the lice or eggs (nits)

254
Q

Lice (P. humanus capitis)- Tx

A

Gamma benzene hexachloride (lindane)

255
Q

Bedbugs (cimex letularis)- appearance

A

Reddish brown insect, 4-5mm, short wing pads but they cant fly

256
Q

Bedbugs (cimex letularis)- epidemiology

A

all over, they feed at night

257
Q

Bedbugs (cimex letularis)- Sx

A

Small red marks to hemorrhagic bullae, they bite in a linear fashion

258
Q

Bedbugs (cimex letularis)- Dx

A

Pattern and location of bites, detecting blood spots on bedding or dead insects themselves.

259
Q

Bedbugs (cimex letularis)- Tx

A

Topical palliatives for pruritis, antihistamines if severe dermatitis.

Dermatology (4 decks)

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