red lesions Flashcards

1
Q

t/f. a vesicle can turn into an ulceration

A

true. but you cant go from an ulceration to a vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

t/f. there is no lymphadenopathy with AI diseases

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epidermolysis bullosa

A

congenital defect in the attachment mechanisms of the epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

tx of epidermolysis bullosa

A

no cure, management: supportive (avoid trauma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

types of lesions in epidermolysis bullosa

A

vesicles and bullae due to minor trauma and oral lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

t/f. viral diseases typically have slow onset

A

false. actue (fast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

features of viral diseases

A

lymphadenopathy (not in recurrent herpes or zoster), ulcers, vesicle stage (except mono)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HHV1

A

herpes simplex 1

typically infects oral region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HHV2

A

herpes simplex 2

typically infects genital region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

herpes simplex oral cavity “history”

A

primary: exposure, often asymptomatic, but if symptomatic: gingivostomatosis
latency period
recurrent: epithelium supplied by sensory ganglion, usually symptomatic, asymptomatic viral shedding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

primary herpetic gingivostomatosis

A

lymphadenopathy with multiple sesicles and ulcers anywhere in the oral cavity
may present subclinical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

primary herpes features

A

pinhead vesicles develop, central ulcerations, yellow fibrin may coalesce into larger ulcers, involves keratinized and nonkeratinized mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

tx for primary herpes

A

acyclovir (zovirax) antiviral: adults - 200mg

resolves in 10-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

recurrent herpes simplex prodrome (early symptoms)

A

tingling, burning, paresthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

recurrent herpes features of vesicles and ulcers

A

small clusters, perioral skin and keratinized oral mucosal surfaces, recur in the same location each time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

t/f lymphadenopathy is present in recurrent herpes

A

false. it is not present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

t/f. primary herpes only occurs on keratinized tissue

A

false. keratinized and non keratinized. recurrent is only keratinized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

tzank cell

A

free floating epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

tx for recurrent herpes

A

effective at prodrome: valacyclovir (valtrex) (Rx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

prophylactic maintenance for recurrent herpes

A

acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

t/f. zoster represents a recurrence

A

true. shingles is a recurrence of varicella (chickenpox)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

t/f zoster only manifests at the terminal end of a nerve

A

false. the entire length of the nerve (shingles=dermatomes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

t/f. shingles is usually unilateral

A

true. follows the peripheral nerve distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

post herpatic nerualgia

A

chronic severe pain in nerve distribution after zoster lesions resolve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HHV4

A

EBV (epstein-barr)/ infection mononucleosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ebv is also associated with these 3 diseases

A

burkitts lymphoma, nasopharyngeal carcinoma, hairy leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

lab features of ebv

A

leukocytosis, lymphocytosis with atypical T cells, positive serology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

oral mucosa features of ebv

A

erythmatous, petechiae on palate, ulcers without vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

etiology of hand foot and mouth

A

coxsackie virus group A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

hand foot and mouth lesions

A

vesicles and ulcers throughout oral cavity

macules and vesicles on hands and feet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

etiology of herpangina

A

coxsackie virus group A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

herpangina lesions

A

vesicales and ulcers on posterior oral cavity: soft palate, uvula, tonsillar pillar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what virus family is measles in?

A

paramyxo (RNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how does measles spread

A

respiratory droplets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

kopliks spots

A

erythmatous mucosal spots annd small blue/white macules in measles that looks like grains of salt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

onset of AI diseases

A

gradual: weeks to months

progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

t/f. AI diseases cant be cured but can be controlled with corticosteroids

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

t/f lymphadenopathy is present in AI diseases

A

FALSE

39
Q

tx for non-microbial mucositis

A

topical: dexamethasone, triamcinolone acetonide
systemic: prednisone
intralesional: trimcinolone acetonide (inject 10-40 mg)

40
Q

prednisone tx for non-microbial mucositis

A

30-60mg A.M.a for 5 days followed by 20mg AM QOD

41
Q

cause of erosive lichen planus

A

immune abnormality involving T lymphocytes
lichenoid drug rxns
GvH rxns

42
Q

features of erosive lichen planus

A

erythmatous ulcers with white striae along periphery
vesicles are rare
bilateral; focal or generalized

43
Q

etiology of pemphigus vulgaris

A

autoabs to intercelluar protein in desmosomes

44
Q

features of pemphigus vulgaris

A

fragile blisters that rupture easily, multifocal

45
Q

nikolsky sign

A

able to induce an ulceration by touching or blowing air on it
sometimes presents in pemphigus vulgaris

46
Q

microscopic features of pemphigus vulgaris

A

tzanck cells

direct immunofluorescence on biopsy

47
Q

2 biopsy specimens needed for pemphigus vulgaris

A

1 submitted in formalin, the other in michels solution

48
Q

tx for pemphigus vulgaris

A

corticosteroids:

dexamethasione, trimcinolone acetonide, prednisone

49
Q

mucous membraine pemphigoid etiology

A

abs against basal lamina (hemidesmosomes) that attack the conjunctiva (eye)

50
Q

where do pemphigoid lesions occur

A

conjunctiva (may cause blindness)

51
Q

tx for mucous memb pemphigoid

A

corticosteroids:

dexamethasone, timcinolone acetonide, prednisone

52
Q

etiology of bullous pemphigoid

A

autoabs against basal lamina

53
Q

t/f bullous pemphigoid is the most common AI blistering condition

A

true

54
Q

BP compared to MMP

A

BP more limited (skin) with NO scarring

55
Q

SLE

A

multisystem diesase with increased activity of B cells and abnormal T cell function

56
Q

CCLE

A

chronic cutaneous lupus erythematosus or “discoid lupus”

confined to skin and oral cavity

57
Q

SCLE

A

subacute cutaneous lupus (intermediate lupus)

58
Q

SLE effects what organs

A

kidneys (kidney failure)

heart (cardiac involvement)

59
Q

CCLE features

A

scaley erythematous patches on skin, scarring and pigmentation

60
Q

SCLE features

A

no scarring or pigmentations, renal changes absent with arthritis

61
Q

chronic desquamative gingivitis presents as

A

diffuse sloughing of gingiva

62
Q

acute erythematous candidosis features

A

most common form
generalized pain, burning and erythema
follows broad spectrum antibiotics

63
Q

chronic erythematous candidiasis is seen in

A

denture wearers

“denture stomatitis”

64
Q

t/f denture stomatitis may not be caused by candida

A

true

65
Q

other features included in denture stomatitis

A

poorly fitting dentures, prolonged wearing of denture, poor hygiene

66
Q

t/f angular chelitis typically occurs with reduced vdo but does not have to be

A

true. (saliva pools in the corner of the mouth)

67
Q

microbes associated in angular chelitis

A

20% candida alone, 20% s. aureus alone, 60% candida and s. aureus

68
Q

microbe causing syphilis

A

treponema palladium

69
Q

primary phase of syphilis

A

chancre at site of innoculation, solitary lesion

70
Q

secondary syphilis

A

cutaneous rash, condyloma lata

71
Q

tertiary syphilis

A

cns and cv probs

72
Q

hutchinsons triad

A

hutchinsons teeth, ocular intersitital keratitis, 8 nerve deafness

73
Q

apthous ulcers have what kind of reaction

A

t-cell mediated immunologic rxn

canker sore

74
Q

types of apthous ulcers

A

minor, major, and herpetiform

75
Q

apthous ulcers are found on what type of tissue

A

non keratinized

76
Q

features of minor apthous ulcers

A

size bt 3-10mm
heal in 1-2wks
no scarring

77
Q

features of major apthous ulcers

A

size bt 1-3cm
heal up to 6 wks
more frequent recurrence
may cause scarring

78
Q

features of herpetiform apthous ulceration

A

non keratinized (herpes in on keratinized)
size 1-3mm
heal in 7-10 days

79
Q

microscopic features of apthous ulcers

A

cant see anything: biopsy is not diagnostic

diagnosis is based on history and clinical features

80
Q

tx of apthous ulcers

A

mild: corticosteroids
major: more potent steroids

81
Q

behcets syndrome

A

serious multisystem disease that consists of apthous like oral ulcers, genital ulcers, ocular inflammation, and skin pustules

82
Q

erythema multiforme

A

acute onset
AI disease with unknown cause with blistering, ulcerative mucocutaneous condition
black necrotic tissue on lips

83
Q

in 50% of cases, erythema multiforme is preceded by

A

herpes or pneumonia

84
Q

forms of erythema multiforma

A

minor, major, and toxic epidermal necrolysis

85
Q

features of erythema multiforme

A
ACUTE ONSET (key feature)
target lesion (erythematous macule)
diffuse painful oral ulcers
86
Q

stevens johnson syndrome

A

more severe erythema multiforme with lesions that involve skin, conjunctiva, oral mucosa, and genital mucosa

87
Q

granulomatosis with polyangiitis

A

granulomas around bvs
glomerulonephritis
systemic vasculitis

88
Q

c-ANCA test

A

test for ab in Granulomatosis with polyangiitis

89
Q

if a pt has chrons, what should you warn them of

A

ulcerations could also manifest in the mouth as well as the GI sys

90
Q

erythroplasia/plakia

A

asymptomatic, persistent, red, or red/white lesion
not ulcerated
microscopically diagnosed

91
Q

erythroplasia can be diagnosed as

A

dysplasia, carcinoma-in-situ, or superficial squamous cell carcinoma

92
Q

what should you include in a differential with pemphigoid

A

pemphigus, erosive luchen planus, lupus, and erythema multiforme

93
Q

how can you clinically differentiate erythema multiforme from pemphigus, pemphigoid, erosive lichen planus, lupus

A

erythema multiforme is acute onset