Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
335 Cards in this Set
- Front
- Back
|
Micro 14
|
Neisseriae: Gonoccus and Meningococcus
|
|
|
causative agent of gonorrhea
|
Neisseria gonorrhoeae
|
|
|
neisseria gonorrhoeae
|
gram negative cocci that is causative agent of gonorrhea
|
|
|
gonococcus usually causes
|
uncomplicated localized cervicitis and urethritis
|
|
|
how does gonococcus attach to epithelia
|
attaches to mucosa through pili and elicits a brisk inflammatory response
|
|
|
ascent of gonococcus into female upper reproductive tract results in
|
inflammation of uterus and fallopian tubes (Pelvic inflammatory disease)
|
|
|
common risk in patients with past history of PID
|
ectopic preg
|
|
|
ascent of gonococcus into male upper reproductive tract causes
|
epididymitis
|
|
|
tenosynovitis syndrome
|
acute dermatitis and arthritis associated with DGI or disseminated gonococcal infection
|
|
|
energy metabolism pattern for Niessaria spp.
|
faculative anaerobes that can use nitrite as an electron acceptor
|
|
|
cell wall differences b/w niesseria and other Gram neg organisms
|
LPS lacks repeating O antigen
|
|
|
asymptomatic carriage of gonococci is more common among
|
women
|
|
|
summarize immune evasion tactics employed by gonococci
|
they go phase and antigenic variation. They are well recognized by our immune system but will change before we produce an adaquate response to them. This is why recurrent infection is a large concern
|
|
|
Opa
|
colony opacity associated proteins that some gonocci express that allows them to be taken in by neutrophils. Strains lacking Opa are associated with PID, DGI and arthritis
|
|
|
effect of gonococci on antibodies
|
gonococci produce a protease that targets IgA1 but not IgA2
|
|
|
explain the process by which gonocci can invade the fallopian epithelium
|
attachment to microvilli of nonciliated cells, which triggers ciliary stasis preventing flushing of bacteria, the ciliated cells die (induced by gonococcal LPS) and the gonococci is internalized into the nonciliated cell whre it replicated and lyses the cell emerging in the subepithelial space
|
|
|
mediates damage to host tissues from gonococci
|
LPS and peptidoglycan which induce production of TNF-a
|
|
|
targets present on gonoccus for circulating antibodies (IgG/M)
|
LOS and protein I
|
|
|
symptoms of cervicitis
|
cervical discharge, bleeding and pain
|
|
|
presumptive evidence of gonococcal infection
|
finding of neutrophils containing G- diplococci
|
|
|
most common media for identification of gonococci
|
thayer-martin or martin-lewis media which contain antibiotics to inhibit non-gonococcal bacteria found in genital tract
|
|
|
result of oxidase test for gonococci
|
positive, if a gram neg diplococci is oxidase positive it is neisseria
|
|
|
reccomended intitial therapy for goocus
|
Beta lactamase resistant cephalosporin --> cefixime or ceftriaxone
|
|
|
Micro 24
|
Syphilis: A disease With History
|
|
|
agent of syphilis
|
treponema pallidum
|
|
|
how do you culture T. pallidum
|
you cant culture it in artificial media
|
|
|
toxins produced by T. pallidum
|
there are none
|
|
|
T. pallidum is sensitive to this antibiotic
|
penicillin, making the disease easily treatable
|
|
|
morphology of Treponema
|
spirochete
|
|
|
cell wall structure of T pallidum
|
similar to G- but without LPS, and with a relatively small amount of surface antigens
|
|
|
why don’t we know much about syphillis
|
we cant culture t pallidum nor do we have a suitable animal model
|
|
|
2 major routes of transmission of syphillis
|
sexual and transplacental
|
|
|
initial encounter and entry of syphillis
|
enters via minute aprasions in skin surface then multiplies locally in an extracellular location, forming an isolated skin lesion. Some escape into lymph and establish a systemic presence
|
|
|
result of initial immune response to area of syphilis inoculation
|
the syphilitic chancre which is painless and seen in primary syphillis
|
|
|
syphilitic chancres and oter genital ulcers are associated with increased risk of
|
HIV transmission or acquisition
|
|
|
primary phase of siphillis lasts
|
2-6 weeks
|
|
|
asymptomatic period following primary syphillis lasts
|
3-6 weeks
|
|
|
secondary syphillis occrus from
|
systemic spread of T. pallidum and replicaton in lymph nodes, liver, joints, muscle, skin and many other sites distant from initial location
|
|
|
resolution and recurrence of secondary syphillis
|
manifestations and rashes of secondary syphillis usually resolve in weeks to months but 1/4 of individuals experience relaps within a year
|
|
|
occurs in 1/3 of patients with untreated secondary spyhillis
|
spontaneous cure
|
|
|
occurs in 2/3 of patients with untreated secondary syphillis
|
progression to latent syphillis
|
|
|
latent syphillis
|
untreated secondary syphillis can go dormant for many years after primary infection
|
|
|
tertiary syphillis
|
1/2 of pt with latent syphillis progress to this phase
|
|
|
hallmarck of tertiary syphillis
|
destruction of tissue caused by inflammatory response to presense of trepomemal antigens
|
|
|
gummas
|
soft mass lesions seen in tertiary syphilis that ccan destroy bone and soft tissue (including organs)
|
|
|
cardiac effects of untreated syphillis
|
can result in vasculitis of vasa vasorum of thoracic aorta and formation of aneurysms
|
|
|
tabes dorsalis
|
staggering ataxic gait often seen in neurosyphillis
|
|
|
charcot joints
|
result rom prolonged tabes dorsalis, seen in knee and ankle
|
|
|
argyll robertson pupil
|
seen in tertiary neurosyphillis, eye will not react to light but will react to object being moved away from eye
|
|
|
premature birth, IUGR, and multiple organ failure is associated with
|
congenital syphillis
|
|
|
hutchinson incisors and mulberry molars
|
tooth abnormalities seen in children born with congenital syphillis
|
|
|
cardiolipin
|
tissue component that patients with syphillis form antibodies to
|
|
|
VDRL / RPR
|
venereal diseases reference laboratory test / rapid plasma reagin. These are nonspecific rapid screening tests for venereal diseases including syphillis
|
|
|
FTA test
|
treponeme specific fluorescent antibody screening
|
|
|
initial treatment for syphillis before penicllin discovery
|
mercury and bismuth for several years
|
|
|
treatment of all stages of syphillis presently relies upon
|
continued sensitivity of T. pallidum to penicillin
|
|
|
standard treatment of syphillis
|
injection of benzathine penacillin
|
|
|
treatment of neurosyphillis
|
high dose IV aequeous crystalline penicillin
|
|
|
treatment of syphillis in penacillin allergic patients
|
doxycycline, tetracycline
|
|
|
treatment of early latent and tertiary syphillis
|
benzathine penacillin G
|
|
|
Micro 27
|
Chlamydiae
|
|
|
characterize the chlamydiae pathogen
|
obligate intracellular gram negative pathogen
|
|
|
how do you culture chlamydiae
|
you don’t
|
|
|
auxotrophy in chlamydiae
|
they require several amino acids and NTPs including ATP found in the host cell. These lead to classification as an energy parasite
|
|
|
2 main chlamydiae organisms
|
C. trachomatis (causes chlamydia) and C. pneumoniae
|
|
|
leading bacterial agent of STDs
|
C trachomatis
|
|
|
C trachomatis and PID
|
C trachomatis is responsible for about 1/2 of PID cases
|
|
|
LGV
|
lymphogranuloma venereum is a biovarient of C. Trachomatis which causes disease of lymph nodes and is infrequently seen in the US, more common among MSM.
|
|
|
leading cause of preventable visual impairment globally
|
trachoma, which is caused by C. trachomatis serovars A-C
|
|
|
entry mechanisms of chlamydicae
|
direct contact with mucous membranes, sexual contact, direct inocultion into the eye, respiratory route via droplet
|
|
|
EB form of chlamydiae
|
elementry body form , infectious Extracellular form that is metabolicly inert
|
|
|
RB form of chlamydiae
|
reticulate body form, intercellular form, that is metaboliclly active
|
|
|
exposure of chlamydiae infected cells to interferon gamma causes
|
persistence which is an altered RB state that displays lowered metabolic rates but remain transcriptionally active.
|
|
|
most damage resulting from C trachomatis infection
|
results from host immune response which results in chronic inflammation and necrosis of infected cells
|
|
|
progression of chlamydia infection in women
|
progression from cervix (cervicitis) to endometrium (endometritis) to fallopian tubes (salphingitis)
|
|
|
progression of chlamydia infection in men
|
progression from urethria to epididymis and prostate, rarely testicles
|
|
|
chronic and repeated infections with chlamydia in women result in
|
tubal factor infertility and PID with elevated risk of ectopic pregnancy
|
|
|
infants born vaginally to mothers infected with chlamydia will develop
|
EB exposure in eyes ears and nose leading to conjunctivitis and pneumonia
|
|
|
NAATs for chlamydia
|
nucleic acid amplification tests such as PCR are now commonly used to detect C trachomatis
|
|
|
procedure for suspected cases of chlamydia
|
must obtain swab of affected mucosal epithelium and assay for both chlamydia and N. gonorrhoeae
|
|
|
first line treatments for C trachomatis serovars A-K
|
azithromycin or doxycycline
|
|
|
Chapter 40
|
HPV and Warts
|
|
|
describe the characteristics of the HPV particle
|
nonenveloped, nonlytic DNA viruses, replicate within squamous epithelial cells
|
|
|
how is HPV spread
|
by direct skin-skin contact, sexual transmission, contact with inanimate objects (fomites)
|
|
|
most common STI
|
chlamydia
|
|
|
most common STI people seek tx for
|
HPV
|
|
|
components of HPV particle
|
L1 and L2 proteins and single copy of circular viral genome
|
|
|
absense of an envelope does what for HPV
|
makes it more environmentally durable, remains infectious longer
|
|
|
criteria for new genotype of HPV
|
more than 10% DNA variance from all other HPVs
|
|
|
cause most common cutaneous warts
|
HPV 1-4
|
|
|
condyloma are usually caused by
|
HPV 6 and 11
|
|
|
why does sexual contact transmitt HPV with high efficiency
|
intimate contact can disturb the epithelial barrier
|
|
|
respiratory papillomatosis
|
seen when HPV is passed from mother to child during birth. This is very bad for child
|
|
|
epidermodysplasia verruciformis
|
HPV infections in AIDS patients. These are longstanding warts that are widespread, if an oncogenic subtype, multiple skin cancers can occur
|
|
|
E1
|
viral protein that maintains the viral DNA as an episome that doesn’t integrate into host
|
|
|
E2
|
binds to specific sequence in viral DNA in a complex with E1. E1 acts as a helicase while E2 as a transcription factor
|
|
|
mediate HPV attachment to epithelial cell
|
heparan sulfated proteins
|
|
|
late in life cycle of keritioncyte, the HPV genome will produce
|
capsid proteins L1/2
|
|
|
high risk HPV type seen in most cancers
|
HPV 16
|
|
|
low risk HPVs found in genital/cervical lesions
|
6 and 11
|
|
|
2 proteins encoded by high risk HPVs that are expressed in all cervical cancer cells
|
E6 and E7
|
|
|
E6
|
expressed in high risk HPVs, inactivate the p53 tumor supressor pathway
|
|
|
E7
|
expressed in high risk HPVs, E7 complexes with Rb family proteins such as p 105-Rb. These normally act as supressors of cell replication but the binding of E7 releases E2F, a transcripton factor which facilitates entry into cell cycle
|
|
|
how can HPV be detected in a lab setting
|
using subtype specific DNA proves to amplify viral DNA using PCR
|
|
|
papanicolaou smear
|
performed to detect cytological abnormalities typical of HPV infections, can identify women with precancerous lesions
|
|
|
nearly all modes of treatment for HPV are
|
ablative
|
|
|
some treatments utilized for HPV lesions
|
liquid nitrogen cryotherapy, caustic keratolytic, cytotoxic chemicals
|
|
|
imiquimod
|
may stimulate immune response to anogenital HPV infection
|
|
|
makes it easier to visualize HPV lesions
|
coating suspected areas with 3-5% acetic acid
|
|
|
Micro Chapter 41
|
Alphaherpesviruses: HSV and VZV
|
|
|
features of the herpesviruses
|
double-stranded DNA genome, icosahedral nucleocapsid, envelope derived from cell membrane of host
|
|
|
almost all individuals get this type of HSV
|
HSV-1
|
|
|
primary spreading mechansim for HSV-2
|
genital-genital contact
|
|
|
most infections with HSV1 and HSV2 are
|
asymptomatic
|
|
|
can asymptomatic individuals spread HSV
|
yes shedding from epithelial surfaces can occur even if lesions are not large enough to be seen
|
|
|
why are herpesviruses susceptable to many environmental factors
|
their membrane envelope
|
|
|
how do alphaherpesviruses bind to cells
|
through interaction of viral glycoproteins with heparin sulfate chains
|
|
|
early genes in HSV
|
centered around replication of viral DNA
|
|
|
late genes in HSV
|
centered around protein synthesis and assembly of progeny
|
|
|
exocytosis of HSV
|
not effeciently released into extracellular space, rather they immediately attach to and penetrate adjacent cells
|
|
|
limitations of host defenses against alphaherpesviruses
|
our natural defenses are sufficient to limit duration/severity of infection but do not prevent latency due to a lack of immune response to latently infected cells
|
|
|
effect of anti herpesvirus antibodies in fighting HSV infection
|
limited, they probably get there too late to do anything
|
|
|
most important immune mechanism for recovery from HSV/VZV
|
cell mediated immune mechanisms
|
|
|
how do HSV/VZV cause damage
|
they destroy the epithelial cells they replicate in causing vesicular lesions that rupture
|
|
|
HSV and encephalitis
|
occasionally HSV1 will pas into the CNS via peripheral nerves, this can cause life threatening encephalitis
|
|
|
diagnosis of HSV
|
usually observation of lesions and adaquate history is enough, but PCR can be done
|
|
|
where do latent HSV particles reside
|
in peripheral sensory/ autonomic nerves
|
|
|
most useful antiviral drugs for herpesviruses
|
acyclovir
|
|
|
penciclovir
|
related to acyclovir and can be used topically but poor oral bioavailability
|
|
|
valacyclovir
|
prodrug of acyclovir with better bioavailability
|
|
|
Pathology Readings
|
Pathology Readings
|
|
|
persistance of viral genomes in cells that don’t produce infectious virus
|
latency
|
|
|
viruses most frequently establishing latent infections in humans
|
herpesviruses
|
|
|
alpha group herpes viruses infect what, and are latent where
|
infect epithelial cells, are latent in neurons
|
|
|
LATs
|
latency associated viral RNA transcripts. These are only synthesized products of HSV during latency. Confer resistance to apoptosis, silence lytic gene expression
|
|
|
how do HSVs avoid antiviral CTLs
|
by inhibiting MHC class I recognition pathways
|
|
|
major infectious cause of corneal blindness
|
HSV-1
|
|
|
major cause of fatal sporadic encephalitis
|
HSV-1
|
|
|
HSV infected cells morphology
|
contain large pink-purple intranuclear inclusions
|
|
|
HSV lesions favoring facial skin and mucosal orifices such as the lips and nose
|
cold sores
|
|
|
gingivostomatisis
|
usually seen in children. This is due to HSV-1. It is characterized by vesicular eruption extending from tongue to retropharynx and is associated with cervical lymphadenopathy
|
|
|
characterized by vesicles on genital mucous membranes and external genitalia that are rapidly converted to superficial ulcerations rimmed with infiltrate
|
genital herpes.
|
|
|
herpes epithelial keratitis
|
occurs in cornea in response to herpes induced cytolysis
|
|
|
herpes stromal keratitis
|
characterized by infiltrates of mononuclear cells around endothelial cells and keratinocytes, this leads to neovascularization and blindness
|
|
|
staining technique that can help to vizualize T. pallidium
|
silver stain
|
|
|
3 main manifestations of tertiary syphillis
|
CV, neuro, benign
|
|
|
most common manifestation of tertiary syphillis
|
CV (80%)
|
|
|
characteristic of benign tertiary syphillis
|
formation of gummas
|
|
|
manifestations of congenital syphillis occuring in first 2 years
|
infantile syphillis
|
|
|
manifestations of congenital syphillis occuring after first 2 years
|
tardive syphillis
|
|
|
sensitivity of RPR and VDRL testing
|
increases from primary to secondary to latent to tertiary
|
|
|
primary syphillis lesions occur where in men, women
|
penis or scrotum (70%) and vulva/cervix (50%)
|
|
|
where are lesions located in secondary syphilis
|
widespread involving oral cavity palms of hands and soles of feet
|
|
|
tertiary syphillis most frequently involves
|
aorta, CNS, liver, bones, testes
|
|
|
why does aortitis occur in tertiary syphillis
|
endarteritis of vasa vasorum of aorta
|
|
|
white gray and rubbery lesions seen in tertiary syphillis
|
gummas
|
|
|
triad of late manifestations of congenital syphillis
|
interstitial keratitis, hutchinson teeth, 8th nerve deafness
|
|
|
why cant chlamydia survive outside the cell
|
unable to synthesize ATP
|
|
|
the elementry body of chlamydia is similar to a spore in what way
|
it is metabolicly inert but able to infect
|
|
|
serotypes D-K of chlamydia
|
urogenital infections and inclusion conjunctivitis
|
|
|
serotypes L1,2,3 of chlamydia
|
LGV lymphogranuloma venereum
|
|
|
serotypes A B C of chlamydia
|
ocular infection in children (trachoma)
|
|
|
pathogenesis of lymphogranuloma venerium
|
initially manifests as small unnoticed papule on genital mucosa. 2-6 weeks later produces tender swollen nodes which can rupture. If un tx it can result in fibrosis and stricture of anogenital tract
|
|
|
features of c trachomatis urethritis
|
almost identical to gonorrhea.
|
|
|
Contraceptives, Cecil's and PPTs
|
Contraceptives, Cecil's and PPTs
|
|
|
all women of childbearing age should take this daily
|
folic acid supplament to avoid NTDs in event of pregnancy
|
|
|
4 most common contraceptive methods used in US
|
1. oral contraceptive pill (31%) 2. tubal sterilization (27%) 3. male condom (18%) 4. vasectomy (9%)
|
|
|
traditional oral contraceptive pill
|
contains both progestin and estrogen
|
|
|
OCP associated with higher rates of breakthrough bleeding
|
triphasic
|
|
|
delivery methods of combined hormone contraceptives that don’t require daily dosing
|
nuvaring and estrogen patch
|
|
|
contraindications for combined hormone contraceptives
|
over 35 and smoke, history of heart or CV disease, liver impairment, hx of thrombosis, suspected breast or endometrial cancer
|
|
|
progestin only method of contraception given in an injectable form
|
depo-provera is progestin only and given IM every 12 weeks.
|
|
|
major side effects of depo shots
|
breakthrough bleeding, weight gain, loss of bone density
|
|
|
depo-provera is indicated for
|
women with contraindiciations to estrogens
|
|
|
copper IUD benefits, side effects
|
highly effective, can be left in for years BUT associated with menstural cramping and heavy flow
|
|
|
Minera IUS
|
IUD that delivers levonoresterel to utereus, thinning the endometrial lining and preventing implantation
|
|
|
contraindications for mirena IUS
|
hx of PID
|
|
|
Plan B
|
emergency contraceptive consisting of a progestin only preperation. Works only in 72 hours following following unprotected intercourse. Ineffective against established pregnancies
|
|
|
combined oral contraceptives work by
|
preventing release of eggs during ovulation
|
|
|
effectiveness of combined oral contraceptives
|
92-99% if used correctly ; 92% as commonly used
|
|
|
progestin only pills work by
|
thickening cervical mucous to block sperm and egg from meeting, prevents ovulation
|
|
|
this contraceptive cant be taken during breast feeding, why
|
combined oral contraceptives, estrogen blocks milk production
|
|
|
"implants" from powerpoint
|
thin hormone releasing rod inserted into upper arm. Works similarly to progestin only pills
|
|
|
side effects of progestin only injectable "depo shot"
|
irregular vaginal bleeding, slow return to fertility
|
|
|
combined injectable contraceptives
|
shot containing both estrogen/progestin that is highly effective 99% but may cause irregular vaginal bleeding
|
|
|
how does the LND IUD (merina) address some of the concerns seen with copper IUDs
|
reduces menstural cramps seen with copper IUD
|
|
|
effectiveness of the male condom
|
98% if used correctly but only 85% as commonly used
|
|
|
female condom effectiveness
|
90% if used correctly , 79% as commonly used. But lets be real has anyone actually ever used one of these things? Do stores even sell them? Seriously doubt it.
|
|
|
diaphragm
|
shallow cup placed over cervix with spermacide. It must be fitted by a physician and has a roughly 90% effectiveness
|
|
|
coitus interruptus
|
penis is removed from vagina. About 75% effective
|
|
|
periodic abstenence
|
calendar based method that centers around avoiding unprotected vaginal coitus during fertile period. Roughly 75% effective
|
|
|
lactation amennorhea
|
during breast feeding the normal ovulatory period doesn’t occur
|
|
|
vasectomy
|
ligation of vas deferens, >99% effective, there is a 3 month delay due to stored sperm, doesn’t effect sexual performance
|
|
|
tubule ligation
|
cutting of fallopian tubes, trapping eggs in ovary, effective immediately >99% effective
|
|
|
transcervical sterilization
|
fallopian tubes irritated and scar tissue grows to block tubes, takes several months for scars to form
|
|
|
Behavioral 21
|
Human Sexuality
|
|
|
testis determining factor gene
|
found in Y chromosome, induces formation of testes from indifferent gonads
|
|
|
when do testes become functional
|
around week 6-7
|
|
|
what substances are secreted by fetal testis
|
androgenic hormones , Mullerian inhibiting substance
|
|
|
wolffian duct
|
develops into male internal/external genetalia , induced by androgens
|
|
|
MIS
|
secreted by fetal testis. inhibits development of mullerian duct (female reporductive genetalia)
|
|
|
effect ioof androgens on fetuses
|
male fetuses deprived of androgens are neurologically/behaviorly demasculinized, while female fetuses exposed to androgens are neurologically and behaviorally masculinized
|
|
|
when do brain changes that result in gender differences occur
|
during second trimester
|
|
|
gender identity
|
sense of self being male/female
|
|
|
gender role
|
expression of ones gender identity in society
|
|
|
sexual orientation
|
persistant and unchanging preference for individuals of different or same sex for love and sexual expression
|
|
|
androgen insensitivity syndrome
|
XY genotype but fetal cells don’t respond to androgens so a female phenotype is expressed
|
|
|
congenital virilizing adrenal hyperplasia
|
CAH, excessive androgen exposure in female (XX) fetus due to a deficiency in 21-OH (90%)
|
|
|
gender identity disorder
|
physically normal with respect to biological sex but feel as if living in body of wrong sex
|
|
|
GID is associated with what prenatally
|
increased exposure to androgens in females, decreased availability of androgens in males
|
|
|
GID and birth order
|
men with GID are more likely to have older brothers than heterosexual men
|
|
|
4 stage model of sexual response
|
excitement plateau orgasm resolution
|
|
|
estrogen and sexual interest
|
not really involved, but lack of estrogen is associated with vaginal thinning and dryness that can make sex uncomfortable for menopausal women
|
|
|
PMDD
|
premenstural dysphoric disorder (PMS) ; can be treated with SSRIs
|
|
|
problems seen in the desire stage
|
hypoactive sexual disire disorder and sexual aversion disorder
|
|
|
changes seen in excitement phase
|
penile/clitoral erection, labial swelling, vaginal lubrication, tenting of uterus, nipple erection, increase in pulse, BP, respiration
|
|
|
problems seen in excitement stage
|
female sexual arousal disorder, male erectile disorder
|
|
|
changes seen in plateau phase
|
increased size/upward movement of testes, secretion of several drops of sperm containing fluid, flushing of chest/face, contraction of outer 1/3 of vagina forming orgasmic platform, further inc in BP/Respiration/Pulse
|
|
|
absense of the plateau phase in men is associated with
|
premature ejaculation
|
|
|
characteristics of orgasm stage
|
forcible expulsion of seminal fluid, contraciton of uterus/vagina, M/F anal sphincter contractions, further inc in BP/resp/pulse
|
|
|
resolution phase
|
muscle relaxtion, in men refractory period with restimulation not possible, minimal refractory phase in women, return to prestimulated state in ~10-15min
|
|
|
effect of dopamine on sexuality
|
stimulatory
|
|
|
effect of antipsychotics on sexuality
|
increase prolactin (due to lower dopamine) , supression of libido, erectile difficulty
|
|
|
effect of serotonin on sexuality
|
negative effect in sexual interest and can delay orgasm
|
|
|
NE effect on sexual function
|
antihpyertensives that act on a/B receptors can reduce libido and cause ED
|
|
|
antihypertensives that are less/more likely to cause sexual function issues
|
more likely: alpha/beta blockers //// less likely: ACE inhibitors
|
|
|
hypoactive sexual desire
|
decreased interest in sex, may be normal individual variation
|
|
|
sexual aversion disorder
|
aversion to /avoidance of sex
|
|
|
female sexual arousal disorder
|
inability to maintain vaginal lubrication despite adaquate stimulation (20% of women)
|
|
|
lifelong male erectile disorder
|
male has never had erection sufficient for penetration :( rare
|
|
|
acquired/secondary male erectile disorder
|
most common of all male sexual disorders
|
|
|
situational male erectile disorder
|
common, inability to maintain erections in some situations but not others
|
|
|
suggests a phychological rather than physical cause of ED
|
rpersistance of morning erections and erections during REM sleep and masturbation
|
|
|
M/F orgasm disorder
|
can be lifelong, acquired, more common in women
|
|
|
premature ejaculation
|
short or absent plateau phase, commonly assoc with anxiety, 2nd most common of male sex disorders
|
|
|
vaginismus
|
painful spasm of outer 1/3 of vagina makes sex or pelvic exam difficult
|
|
|
dyspareunia
|
pain associated with sex, more common in women
|
|
|
sensate focus exercises
|
aimed at decreasing performance anxiety with sex, pt instructed to concentrate on nongenital menas of arousal
|
|
|
can help patients learn what stimuli and techniques are most effective in achieving arousal/orgasm
|
masturbation
|
|
|
squeeze technique
|
man is taught to concentrate on sensations that preceede orgasm, asks partner to press on coronal ridge just prior to orgasm to gain more time
|
|
|
useful to treating premature ejaculation
|
SSRIS
|
|
|
sidenafil
|
PDE 5 inhibitor, blocks enzyme that destroys cGMP (PDE 5). cGMP is a vasodilator secreted in penis with sexual stimulation.
|
|
|
contraindications for sidenafil
|
"don’t take viagra if youre taking nitrates for chest pain"
|
|
|
other medical techniques for ED
|
newer PDE-5 inhibitors and intracorporeal injection of vasodilators and PG E1
|
|
|
men with history of this are likely to have ED and decreased sexual interest
|
MI
|
|
|
men with this condition are likely to have ED
|
diabetes
|
|
|
major causes of ED in men with diabetes
|
vascular changes and neuropathy
|
|
|
changes in sexuality with age
|
while older individuals still are sexual, men have slower erection, diminished intensity of ejaculation, and longer refractory period. Aging women have issues with vaginal dryness
|
|
|
riskiest sexual practice for HIV transmission
|
anal intercourse
|
|
|
paraphalias
|
preferencial use of unusual objects of sexual desire/engagement in unusual sexual activity over 6 month period with impairment in occupational/social fxn
|
|
|
exhibitionism
|
revealing ones genitals to unsuspecting women
|
|
|
fetishism
|
contact with inanimate objects , transvestic is wearing womens clothing
|
|
|
frotteurism
|
rubbing ones penis against clothed nonconsenting woman
|
|
|
pedophilia
|
engaging in behaviors with children less than 14, pedophile must be 16 and 5 years older than victim,
|
|
|
most common paraphalia
|
pedophilia
|
|
|
sexual masochism
|
receiving physical pain/humiliation
|
|
|
sexual sadism
|
giving pain/humiliation
|
|
|
voyeurism
|
secretlye watching other people engaging in sex
|
|
|
corpophilia
|
feces
|
|
|
klismaphilia
|
enemas
|
|
|
necrophilia
|
dead bodies
|
|
|
partialism
|
only involving parts of body
|
|
|
telephone scatologia
|
calling random women to talk about sex
|
|
|
urophillia
|
urine
|
|
|
zoophilia
|
animals
|
|
|
Sexual Response Cycle PPT
|
Sexual Response Cycle PPT
|
|
|
length of excitement phase in men/women
|
several minutes to hours, increase in 3min-30s prior to orgasm for both men and women
|
|
|
length of orgasm phase in men/women
|
3-15 s for men and women
|
|
|
length of resolution phase in men/ women
|
10-15 min, if no orgasm 1/2 to 1 day. Book says women have shorter refractory period
|
|
|
skin changes in men through sexual cycle
|
prior to orgasm inconsistant flushing, most pronounced during orgasm
|
|
|
erection
|
erection occurs in 10-30s due to vasocongestion in corpora cavernosa, loss of erection can occur with asexual stimulus, with heightened excitement size of glands and shaft increase,
|
|
|
ejaculation
|
emission 3-4 short contractions of vas and seminal vesicles, prostate //// ejaculation marked by .8s contractions resulting in spurts 12-20 in (age 18) or seepage (age 70)
|
|
|
changes in penis during resolution phase
|
partial involution in 5-10s with variable refractory pd, full return to prearousal size in 5-30m
|
|
|
changes to testis during sex response cycle
|
tightening/lifting of scrotal sack and elevation with excitement, 50% increase in testicular size, flattening against perineum signals ejaculation imminent , no change in orgasm, return to normal in 5-30 minuts following orgasm
|
|
|
when is the cowpers gland active
|
during excitement mucoid fluid are secreted
|
|
|
HR in males reaches ________ in excitement, orgasm
|
175-180bpm
|
|
|
BP raise in males during excitement, orgasm
|
systolic 20-80 ; diastolic 10-40 for excitement ///// in orgasm 40-100 in systolic and 20-50 in diastolic
|
|
|
respiration during excitement orgasm for males
|
increased to as high as 40 rpm
|
|
|
rectal changes during orgasm
|
rhythmic contractions
|
|
|
female skin changes
|
just prior to orgasm sexual flush on abdomen, ant chest wall, face, neck ; peaks with orgasm, subsides in resolution
|
|
|
female breast changes
|
nipple erection in 2/3 of women during excitement, with aeriolar enlargment/// breast may become tremulous in orgasm
|
|
|
clitoral changes through cycle
|
enlargement similar to male erection, prior to orgasm shaft retracts . Returns to normal in 5-10s after orgasm
|
|
|
nullaparious and multiparrous changes in labia with sex
|
nullaparious : elevation and flattening against perineum prior to O //// multiparous: congestion and edema with return to normal taking 10-15m
|
|
|
changes to labia minora with sex
|
size inc 2-3x, change from pink to deep red before O, contracts with O, returns to norm in 5m
|
|
|
vaginal changes with sex
|
in excitement, color changes to dark purple, transudation10- 30s after arousal , elongation and balooning of vagina, contractions of proximal vagina at 0.8s intervals occur during O, in resolution phase maje ejaculate pools in upper 2/3 , congestion dissipates in seconds, if no O 20-30m
|
|
|
uterine changes with sex
|
ascention into false pelvis during excitement , contractions similar to labor begin before O, peak during O then cease and return to normal
|
|
|
bartholins glands
|
secrete lubricating fluid during excitement
|
|
|
Sexual Dysfunction PPT
|
Sexual Dysfunction PPT
|
|
|
categories of organic ED
|
peripheral and central
|
|
|
peripheral causes of ED
|
vascular, neural (peripheral neuropathy), anatomical, endocrine (gonadal hormones, receptor issues in the penis)
|
|
|
central causes of ED
|
neural lesions, endocrine (pituitary),
|
|
|
Generalized central ED
|
lack of sexual arousal or age related decline , generalized inhibition or chronic d.o of intimacy
|
|
|
psychological central ED
|
depression, stress, loss of partner
|
|
|
situational ED can be
|
partner related, performance related, environment related
|
|
|
leading complaints for sexual dysfunction
|
loss of desire, inadaquate arousal leading to ED/vaginal dryness, impaired orgasm,
|
|
|
most common male sexual dysfunction
|
ED
|
|
|
when is ED most bothersome for males
|
in 50s and 60s
|
|
|
treatment for ED
|
PDE5 inhibitor, dopamine
|
|
|
non-coital sexual pain disorder
|
recurrent or persistant genital pain caused by non-coital sexual stimulation
|
|
|
DSM 5 for female orgasm disorder
|
marked delay, marked infrequency, absense of orgasm (75-100%) of time, minimum of 6 months, not explained by nonsexual mental disorder/substance/partner violence/etc…
|
|
|
DSM 5 for ED
|
difficulty getting/maintaining erection 75-100% of time or marked decrease in rigidity, 6 months, significant distress, not better explained by other mental/drug/relationship issues
|
|
|
three Cs method
|
address sexual dysfunction in pt by targiting chronicity, communication, commitiment
|
|
|
Mosby p108-110 Sexual Maturation, Tanner Scale
|
Mosby p 108-110 Sexual Maturation
|
|
|
Tanner Staging for Female Breast Development
|
1. preadolescent, only nipple raised above level of breast//// 2. budding stage, elevation of areola, inc diameter, surrounding area slightly raised /// 3. breast and aerola enlarged ///// 4. increasing fat deposits, aerola develops a secondary elevation ///// 5. mature stage aerola part of general breast contour
|
|
|
Tanner Staging for Female genital Development
|
1. preadolescent no pubic hair growth/////2. initial hair growth pigmented, straight, along medial labial border/////3. sparce, dark visibly pigmented //////4. hair coarse and curly, abundunt but less than adult////5. lateral spreading in triangle pattern toward medial thighs////6. in 10% of women futhter extension occurs
|
|
|
Tanner Staging for Male gential development
|
1. preadolescent ////2. enlargment of scrotum and testes skin of scrotum becomes darker redder and wrinkled/////3. penis enlargment especially in length further scrotal enlargment /////4. further enlargment, sculpturing of glans increased scrotal pigmentation,/////5. adult stage
|
|
|
onset of puberty in females occurs at what stage
|
when breast or hair reach stage 2
|
|
|
completion of puberty in females occurs when
|
breast stage 4 or hair stage 5 is reached
|
|
|
when does menarche usually occur
|
SMR 4 or breast 3-4
|
|
|
When does ejaculation begin to occur in males
|
stage 3 with semen appearing between 3-4
|
|
|
More Pathology
|
Male and Female Genital Tract / STIs
|
|
|
HSV in women most commonly affects
|
cervix, vagina, vulva
|
|
|
HSV serotype typically resulting in oropharyngeal infection, genital
|
HSV-1 ; HSV-2
|
|
|
by age 40 _________% of women are seropositive for HSV2 antibodies
|
30% , wrap it up fellas
|
|
|
lesions from HSV develop how long after transmisssion
|
3-7 days
|
|
|
progression of HSV lesions
|
papules --> vesicles ---> ulcers
|
|
|
tranmission of HSV occurs mainly during
|
active phase
|
|
|
changes in female vaginal microflora is a common cause of
|
candidiasis
|
|
|
permissive changes or conditions for development of vaginal candidiasis
|
diabetes, antibiotics, pregnancy, compromised neutrophils
|
|
|
trichomonas vaginalis
|
protozoan transmitted by sexual contact that causes yellow frothy vainal discharge, discomfort, dysuria, dysparenuia, and a strawberry cervix
|
|
|
strawberry cervix is associated with what STI
|
trichomonas vaginalis
|
|
|
implicated as main cause of bacterial vaginosis
|
gardnerella vaginalis
|
|
|
presents with thin green-grey fishy vaginal discharge
|
gardnerella vaginalis
|
|
|
pelvic pain, adnexal tenderness, and vaginal discharge resulting from infection that originated in vulva/vagina
|
PID
|
|
|
2 most common causes of PID
|
neisseria gonorrhoeae and chlamydia
|
|
|
acute complications of PID
|
peritonitis and babcteremia which can lead to bacteremia and endocartitis as well as meningitis and suppurative arthritis
|
|
|
chronic sequellae of PID
|
infertility, tubal obstruction, ectopic pregnancy, pelvic pain, intestinal obstruction
|
|
|
Cecils 68
|
Male Endocrinology
|
|
|
most common congenital cause of testicular failure
|
klienfelter syndrome
|
|
|
myotonic dsytrophy can cause
|
primary gonadal failure
|
|
|
cryptorchidism
|
spontaneously corrects in most cases but exposure to intra-abdominal temperatures can damage spermatogenesis
|
|
|
bilateral anorchia
|
rare condition where external genetalia form but testicular tissue dissappears
|
|
|
differentiating bilateral anorchia and cryptochidism
|
bHCG stimulation will induce increase in testosterone in patients with cryptochidism but not bilateral anorchia
|
|
|
testicular feminization
|
absense of androgen receptor (AIS) leading to female phenotype in an XY genotype
|
|
|
lack of 5a reductase enzyme can result in
|
bifid scrotum or hypospadias
|
