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KEY NOTES WK 3 Flashcards

1
Q

atopic dermatitis comorbid with

A

allergic asthma and allergic rhinitis

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2
Q

sx of atopic dermatitis

A

pruritis (itch), eczematous dermatiits

facial and extensors in infants

flexural in older

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3
Q

Ig_ and atopic dermatitis

A

IgE

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4
Q

pathogensis of atopic dermatitis

A

skin barrier defects- filagrin genes

altered immune, cytokines, t cells

xerosis

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5
Q

filaggrin defieicny sx in atopic dermatitis

A

ichthyosis vulgaris, keratosis pilaris, and hyperlinear palms.

increases transepidermal water loss

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6
Q

Th_ in atopic dermatitis and Ig_

A

Th2, IgE, eosinophilia

also Th1

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7
Q

exogenous things that can worse atopic dermatitis

A

scratching, proteases from dust mites, staph aureus

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8
Q

genes in atopic dermatitis and what complex is it involved in

A

Filaggrin gene is found on chromosome 1q21 (minority of patents have FLG null mutation, its usually immune mediated reduction in epidermal differentiation)

which is involved in epidermal differentiation complex

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9
Q

acute vs chronic lesions of atopic dermatitis

A

acute: epidermal spongiosis (edema), T cell with CLA, mast cells, dendritic APCs (langerhans)

chronic: lichenified, hyperkeratosis, minimal spongiosis, more IgE langerhans, macrophages, fully granulated mast cells

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10
Q

what immune cell is absent in atopic dermatitis

A

neutrophils

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11
Q

2 key cytokines causing atopic dermatitis inflammation and causing a Th_

A

TSLP and IL-33 (Th2)

also IL22 IL17 IL4 and Il13

also Th1 cytokines INFy

IL5 for eosinophils

Chemokines: CTACK, CCR4, CCL17,

FUCK ETC…..

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12
Q

severity of atopic dermatitis correlates with

A

evels of thymus and activation-regulated cytokine (TARC)

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13
Q

which cytokines down regulate filaggrin expression in atopic dermatitis

A

TSLp, IL4, IL13

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14
Q

pruritis in atopic dermatitis because

A

allergen induced release of histamine

T cell cytokines: IL-31, stress induced neuropeptides (substance P and CGRP), proteases , eicosanoids (from arachidonic acid), eosinophil-derived proteins (major basic protein and eosinophil derived neurotoxin)

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15
Q

hypersensitivity rxn in allergic contact dermatitis

A

type IV (delayed)

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16
Q

steps of allergic contact dermatitis

A

sensitization (hapten binds skin and forms complex)

need subsequent exposure to get inflammatory response

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17
Q

gold standard test for allergic contact dermatitis

A

patch testing

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18
Q

examples of allergic contact dermatiis

A

nickle, cosmetics, gragnace, textiles, rubber gloves, glue

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19
Q

allergic contact dermatitis sx

A

pruritic, eczematous, edema, erythema, vesicle or papule then can be lichenification and scaling if chronic

geometric, linear or focal pattern

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20
Q

2 phases of allergic contact dermaitis

A
  1. sensitization phase: initial contact with allergen to develop immunologic memory, need sufficient exposure of sensitizing chemical
  2. elicitation phase; re-exposure triggers inflammatory rxn to minute quantities of allergen
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21
Q

how do haptens play a role in allergic contact dermatitis

A

hapten protein complex forms = antigen –> trigger immune response

keratinocytes release GM-CSF, TNFa, IL1, IL8, IL18 upon hapten exposure

langerhan and dendritic cells uptake antigen and express on HLA for T cells which get skin homing antigens

T cells become memory so then next exposure will react

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22
Q

elicitation phase of allergic contact dermatitis

A

Inducible Skin-Associated Lymphoid Tissue (iSALT)

effect T cell recruitment (APCs on langerhans and dermal dendritic cells)

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23
Q

irritant dermatitis differs from allergic contact dermatitis

A

ACD need complete avoidance

ACD need sensitization phase

irritant predisposes to ACD

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24
Q

treat irritant dermatitis

A

emollients

hardening= disappearance of sx

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25
irritant dermatitis examples
wet to dry and heat cold, soaps, detergents, hand washing, cleaners, occupational, gloves
26
irritant dermatitis cause
physical damage to epidermis, temporally more immediate than ACD damage keratinocytes
27
steps in irritant dermatitis
1. epidermal insult (i.e. solvents removed lipids) 2. danger signals (keratinocytes release alarmins- activate TLR, NF-kB) 3. potential for allergic sensitization
28
seborrheic dermatitis sx
greasy, scaly patches and plaques on scalp, face, ears, intertrigous areas
29
cause of seborrheic dermatitis
malassezia (oleic acid, aryl hydrocarbon receptor), sebaceous glands from hormonal changes , cold and dry, immunocompromised (AIDs, Parkinson) decreased by sun
30
Ig_ in seborrheic dermatitis
IgA and IgG
31
ifnalmamtory cytokines in seborrheic dermatitis
interleukin (IL)-1α, IL-1β, IL-4, IL-12, TNFα, and (IFN)- γ
32
malassezia species that cause seborrheic dermatitis and what receptor they act as agonist for
Malassezia globosa and Malassezia restricta aryl hydrocarbon receptor (AhR) --> Th17 cells --> inflame
33
aryl hydrocarbon receptor (AhR) from mallassezia activate what in seborrheic dermatitis
Differentiation of T-helper 17 cells.
34
hyperproliferation of epidermis in
serbohreic dermatitis and psoriasis
35
bacterial interference
resident microbes prevent colonization by pathogenic microbes via: * (1) Competition for receptors or binding sites on host cells * (2) Competition for resources like nutrients *(3) Mutual inhibition by metabolic or toxic product release
36
urethra microbiom
urine not sterile same as on perineum
37
vaginal microbiome change with age
after birth- lactobacilli until puberty- cocci and bacilli puberty- lactobacilli return and group B strep and clostridium, gardnerella... menopasue- lactobacilli decrease
38
cervical mucous has
lysozymes (antibacterial)
39
if remove lactobacilli with antibitioccs can get
yeast colonization --> vaginitis
40
placenta and uterus
not sterile, good bacteria for pregnancies
41
bacterial vaginosis (dysbiosis) from increase in what species
gardnerella vaginalis and mycoplasma hominis
42
bacterial vaginitis sx
Vaginal malodor, increased white-gray discharge, possible dysuria and pruritus
43
complications of bacterial vaginosis
PID, pregnancy complications
44
chlamydia trachomatis has 2 morphologies
replicate body (replicative) and elementary body (infective)
45
different serotypes of chlaymdia vs for chlaymida lymphogranuloma venereum
chlamydia- serotypes D-K LV- serotypes L1-L3
46
transmission of chlamydia
sex, mucus, vaginal delivery
47
sx of chlamydia
female often asymptomatic cervicitis, discharge...
48
complications of chlamydia
PID, neonatal conjunctivitis reactive arthritis (cant see cant pee cant dance w me)
49
Chlamydia Trachomatis – Lymphogranuloma venereum (LGV)
genital ulcers --> lymphangitis and scars
50
Neisseria gonorrhea have what that virulence factors and which one makes have genetic variability
lipooligosacchardie many plasmids for genetic variability opa and pilin proteins for phase variation and prevent antibody binding and immunological memory
51
gonorrhoea phase variation via
opa and pilin proteins
52
gonorrhoea tramsision
sex, mucos, vaginal delitery
53
gonorrhoea sx
urethritis (women asymptomatic usually) extra genital: pharyngitis, conjunctivitis, Gonococcal Dermatitis-Arthritis Syndrome
54
complications of gonorrhea
PID, infertile
55
Treponema Pallidum Pallidum - Syphilis stages
1st stage: painless chancre (sore) into ulcer 2nd stage: ulcer disappears and get rash on palms and soles latent stage tertiary: granuloma, cardiac, and neurologic sx
56
congenital syphilis
impact baby bones, anemia, hepatosplenomgealy, brain....
57
Haemophilus ducreyi sx
* PAINFUL pustule that erodes into ulcer
58
mycoplasma genitalium and ureaplasma urealyticum morphology sx
no cell wall urethritis, cervicitis (PID, infertile)
59
Trichomonas vaginalis sx
purulent yellow discharge with strawberry cervix, urethritis
60
STI comnplications
PID (chlamydia and gonorrhea esp.) (BV- flora changes)
61
Candida albicans virulence
dimorphic- yeast (spore) (at ph <6) or hyphae (at ph >7- more invasive) biofilm formation phenotypic switching, quorum sensing
62
Candida albicans sx
Vulvovaginal candidiasis: vulvar pruritus, burning, irritation, often without discharge or unusual odor or cottage cheese
63
HPV (STI) causes
genital warts or genital cancer if high risk strain
64
HSV-2 is aka
genital herpes
65
HSV-2 sx
urethritis congenital and perinatal infextion latent in local sensory ganglia
66
HIV 3 key viral enzymes
protease, reverse transcriptase, and integrase used to insert its DNA into host cell genome
67
transmission of HIV
sex, congenital, blood, trauma
68
ligands for transcyotis of HIV
GP120 ligand and GP41 co-ligand to attach to the galactosyl ceramide lipid on the new host’s epithelium
69
transmigration of HIV via
DC-SIGN
70
lymph node transmission of HIV
XR4 ligand and CXCR4 receptor on CD4+ T cells or R5 ligand and CCR5 receptor on macrophage
71
how does HIV get activated and replicate
activate if detects antigens or other STIs activate T cells and macrophage replicate and release new virions (T cells die, macrophages survive) ***will stay latent in T cell until stimuli like a cytokine, inflame, APC, to become activated
72
where does HIV remain latent before activated and what cell does it affect and deplete the most
CD4+ T cells
73
stages of HIV
stage 1- lymphadenopathy stage 2- latent CD4+ <500ul stage 3- advanced stage 4- AIDS (opportunistic infection), CD4+ <200c/u;l
74
how does HIV become AIDs
get AIDs if CD4+ cells are so depleted and then become more suscpecitible to getting another infection
75
HIV encephalopathy
invade CNS; i.e. dementia
76
which cancer is easy to screen for with Pap smear and HPV test
cervical cancer
77
central hypothalamic pituitary function causing disorders of reproductive tract
GnRH secretion body fat, stress causes amenorrhea
78
ovarian disorders and sx
I.e. PCOS, no viable follicles, dont respond to gonadotropins hirsutism, infertility, anovulation, abnormal bleeds
79
common causes of uterine disorder/ endometrail dysfunction
homronal fibroids (myomas) - tumor of mymoetrium endometrial cancer sx abnormal bleeds
80
pelvic infections from
gonorrhea, chlamydia, anaerobic bacteria scarring can cause infertility elevated WBC, fever
81
diagnostic approach to amenrrhea; 3 steps
1. rule out pregnancy 2. TSH (thyroid) and prolactin (pituitary) 3. further tests based on history and physical exam
82
uterine disorders cause
i.e. damage stem cells that make endometrium (i.e. curettage, post part, chronic inflam) can cause amenorrhea and lining < 5mm
83
treat uterine disorders and make functional endometrium
progesterone and estrogen therapy
84
differentiate btwn endometrial vs endocrine causes of uterine disorders
endometrial: no withdrawal bleed after hormonal therapy endocrine: withdrawal bleed (insufficient cyclic progesterone and estrogen stimulation)
85
primary vs secondary ovarian disoders
primary- premature ovarian insuffiecieny secondary-lack of gonadotropin stimulation
86
premature ovarian insufficiency (lose ovarian follicles --> fail) from
genetics, metabolic, autoimmune, exogenous chmeicals
87
secondary ovarian insufficiency from
lack of gonadtopin stimulation from the brain --> low estrogen and progesterone prodcution i.e. pituitary disorder or hypothalamic (stress, exercise)
88
primary ovarian insufficiency
< 40 yoa (follicular atresia) --> failure
89
primary ovarian insufficiency hormones
high FSH and LH (no feedback) low estrogen (no follicles viable)
90
symptoms of primary ovarian insufficiency
(estrogen defincieny/menopasuse sx) hot flashes, vaginal atrophy, decrease bone density
91
associated conditions with primary ovarian insufficiency
autoimmune polyglandular syndrome diabetes, hypothyroid genetics (FMR1, tuner, Y chromosome mocaism)
92
chronic anovulation sx and effects
follicles present, but dont mature and ovulate amenorrhea w intermittent bleeds increased estrogen exposure risks (without progesterone) (endometrial hyperplasia and carcinoma)
93
cause of chronic anovulation
thyroid hyperprolactinemia (decreases GnRH) PCOS pituitary (Sheehan, trauma) and hypothalsmic
94
sheehan syndrome causing chronic anovulation
pituitary enlarges during pregnancy from lactotroph hyperplasia and then postpartum hemorrhage and hypotension and pituitary infarction cant lactate postpartum (prolactin deficient) amenorrhea (GnRH deficient) fatigue, hypotesnion, hypoglycemia (lose ACTH, TSH)
95
hypothalamic amenorrhea homrones
low GnRH pulsattility --> decrease LH and FSH --> decrease progesterone and estrogen rules out hyperprolactineamia and hypothyroidism (prolactin, TSH, free T4)
96
high prolactin suppresses
GnRH
97
hypothryoid cause anvoluation
high TRH stimulates prolactin --> suppress GnRH
98
treat hyperprolactineamia
dopamine agonist
99
cause amenorrhea
dysgenesis (abrnoaml uterus and vagina from genes) imperforate hymen or transverse vaginal septum endometrail adhesion, scarring from curettage, uterine tuberculosis (Asherman)
100
primary dysmenorrhea
menstural pain with no structural abnormalities endometrial necrosis --> make prostaglandins --> myometrail contractions --> muscle hypoxia and pain fiber irritated
101
which substance causes pain in primary dysmenorrhea
prostaglandins from endometrial necrosis
102
endometriosis (endometrial tissue outside uterine lining) from
a) retrograde menstruation through Fallopian tubes into pelvic cavity, and/or b) metaplasia of celomic mesenchyme into endometrial tissue, and/or c) vascular or lymphatic dissemination of endometrial “seeds”
103
endometriosis inflammation triggers
cytokines and angiogenesis (new blood vessels with pain fibers) scarring adhesions
104
pelvic inflammatory disease (PID)
infection of upper genital tract (i.e. STI) can lead to scarring and adhesions if not managed
105
ovarian masses
non-neoplastic cyst neoplastic
106
prolpase and cause (which muscle)
many types but I,e uterus through pelvic floor or vaginal introitus (3 degrees ie.. 2nd degree is cervix through introits) dysfunction of pelvic floor --> levator ani esp if old and parous (given birth)
107
abnormal uterine bleeding causes
i.e. polyp, leiomyoga, adenomyosis, coagultpathy, ovculatory, malignancy, iatrogenic (IUD)
108
benign uterine masses (3)
endometrial polyps -->outgrowth of endometraila glands into lumen of uterus adenomyosis --> endometrial gland in myometrium (downward growth) leiomyoma (fibroids) - tumor in myometrium
109
adenomyosis vs endometrial polyp
EP= endometrial outgrowth into lumen of uterus adeno= down growth of endometrial glands to myometrium
110
endometrial hyperplasia what ratio what hormone
increase gland: stroma ratio from unopposed estrogen (I,e, chronic anovulation, peripheral androgens from obesity, estrogen therapy) can progress to endometrial carcinoma
111
cervical dysplasia vs cervical cancer
Cervical dysplasia: Precancerous changes in cervical cells. Cervical cancer: Malignant progression of dysplastic cells.
112
risks for cervical dysplasia and cancer
HPV (high risk 16, 18...) tobacco immunosuppression (HIV) multiple sex partners
113
cervicitis from
changing vaginal microbiome - i.e. cyclic hormonal change pH and flora with or without infection (Pap smear)
114
cervical atypia and dysplasia what type of cell causes
squamous cell HPV (16, 18), smoking, sex, immunosuppress
115
HPV mechanism to cause cervical dysplasia
HPV hijacks epithelia cells to make viral particles and inactivates tumor suppressor genes
116
vaginitis and vulvitis from
changes in microbiomes (pH, hormones, exogenous trauma or pathogen)
117
infectious vs non infectious vaginitis
infectious: Bacterial vaginosis, vulvovaginal candidiasis, trichomoniasis non infectious: chemical, atrophic vagnitis, allergic vaginitis, foreign body
118
vulvo/vaginal malignancy type of cell
squamous cell carcinoma
119

BMS250 (52 decks)

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