Rh/ Vulvovaginitis Flashcards
Rhesus Factor
general
Rhesus factor
Inherited lipoprotein on the surface of RBCs
Several Rh antigens - Rh (D)
Presence of Rh (D) = Rh +; Absence of Rh = Rh-
Rh (D) Negative vs Positive
If mother AND father are Rh (D) positive = fetus will be Rh (D) +
No intervention required
If both mother AND father Rh (D) negative = fetus will be Rh (D) –
No intervention required
If mother is Rh (D) negative and father is Rh(D) positive -> Fetus can be Rh(D) positive
RhoGam protocol to prevention of maternal antibodies against fetus
1st pregnancy
In the first pregnancy
If the mother is Rh NEGATIVE and the baby is Rh POSITIVE,there is Rh incompatibility
The mother will create anti-Rh (D) antibodies
2nd pregnancy
Complications for baby
In the second pregnancy
The mother’s IgG anti-Rh (D) antibodies will travel through the placenta and attack the baby (if this baby is also Rh POSITIVE - ie has the antigen on it’s RBCs)
Can lead to fetal hemolytic anemia, or in severe cases, hydrops fetalis
Rh Alloimmunization
Alloimmunization
An immune response when exposed to foreign antigens which stimulates production of immunoglobulin G (IgG) antibodies
Maternal Rh (D) Alloimmunization
Rh (D) negative mother exposed to Rh (D) positive fetal blood
Occurs during events where maternal/fetal blood can mix:
Miscarriage, therapeutic termination, ectopic pregnancy, antenatal bleeding, abdominal trauma
Procedures: chorionic villus sampling (CVS), amniocentesis, external cephalic version (ECV)
Screening for Rh(D) in Pregnancy
First prenatal visit
All pregnant women should be screened for the ABO blood group & Rh (D) antigen
Prevention of Rh(D) Alloimmunization
And when to do it
Anti-D immunoglobulin (Rhogam) injection
Administered to women exposed or at high risk of being exposed to Rh (D) + RBCs
Suppresses immune response and antibody formation
Dose: 300 µg IM injection
Protect against maternal alloimmunization from 15mL of fetal RBCs/ 30mL of fetal whole blood
Rhogam administration protocol
28 weeks: Administer to all patients, if Rh negative
40 weeks: If more than 12 weeks have elapsed since Rhogam administration, administer again
Postpartum: If infant Rh (D) +
Recommend 72 hours after delivery, however shown to be effective up to 28 days after delivery
Fetomaternal bleeding
As little as 0.1 ml of Rh+ cells can cause sensitization !
Evaluation of Fetomaternal Hemorrhage
Rosette test
Positive
Kleihauer-Betke test (flow cytometry)
Measure amount of fetal hemoglobin transferred to maternal bloodstream
Aid in determination of number of vials of Rhogam administered
1 vial contains 300mcg which protects against 30 mL of whole fetal blood
Maternal Rh (D) Alloimmunization
Hemolytic Disease of the Fetus & Newborn
HDFN or erythroblastosis fetalis
Destruction of RBCs of the fetus or neonate by maternal IgG antibodies
Clinical manifestations
Mild self-limiting (hyperbilirubinemia within first 24 hours of life, symptomatic anemia without circulatory collapse)
Severe (Hydrops Fetalis)
Skin edema, pleural or pericardial effusion or ascites
Rh(D) Summary
Routine screening
ABO, Rh (D)
Rhogam Protocol
300mcg IM injection
28 weeks, postpartum & Fetomaternal hemorrhage
Fetomaternal hemorrhage evaluation
Kleihauer-Betke test
HDFN
Mild – severe manifestations
Primarily dependent on transportation of maternal antibody concentrations
Management of Rh Alloimmunized Women
Step 1: Determine Fetal Risk
Step 2: Follow Maternal Anti-D Titers
Step 3: Assess for Severe Anemia in Fetus
Step 4: Determine Obstetric & Delivery Plan
Vulvovaginitis
general
Term used to describe an acuteinflammationof the vulva and vagina that results from disruption of the normal vaginal environment (flora)
Epidemiology
~75% of women will have at least 1 episode of vulvovaginitis in their lifetime
Etiology
Infectious
Bacterial vaginosis (BV)
Candida albicans
Trichomonas vaginalis
Non-infectious
Lichen simplex chronicus
Irritant contact dermatitis
Lichen sclerosus
Vaginal Flora & Pathogenesis of Vulvovaginitis
Stratified squamous epithelium of the vagina is rich in glycogen
Glycogen is metabolized to lactic acid byLactobacillus:
Creates an acidic environment (pH3.8-4.2)
Maintains the normal vaginal flora
Inhibits growth of pathogens
Vulvovaginitis results from a disruption of the vaginal flora
↓ or ↑estrogen levels
Alkalinization of the vaginalpH
Menstrual blood
Semen
Hygienic products (douching)
↓Lactobacillusfrom broad-spectrum antibiotic use
Bacterial Vaginosis (BV)
Also referred to asGardnerella vaginalis (most common etiology)
Etiology & Pathophysiology
↓Lactobacillus →↑pH→overgrowth of anaerobic bacteria:
Gardnerella vaginalis
Non-spore forming, non-motile, gram-variablebacillus
Creates a biofilm that then allows other opportunistic bacteria to grow within the vagina
Produces vaginolysin,a pore-forming toxin affectinghuman cells
Anaerobic bacteria produce enzymes →break down vaginal peptides into amines, leading to:
Vaginal transudation (vaginal secretions)
Squamous epithelial cell exfoliation
Odor
BV
Risk Factors
Unprotectedsex
↑ Number of sexual partners
Other sexually transmitted infections (STIs)
Douching
Bathing in a bathtub (particularly bubble baths)
BV
Dx and labs
Higher than normal vaginal pH (> 4.5)
Saline wet mount
Clue cells (bacteriaadhering to epithelial cells)
Whiff-amine test
Presence of a fishy odor when 10% potassiumhydroxide (KOH) is added to a sample of vaginal discharge
Amsel Diagnostic Criteria (3 of 4 must be present)
Thin, white-gray discharge
VaginalsecretionpH> 4.5
Positive amine whiff test (fishy odor)
Presence of clue cells
Candidal Vaginitis
Etiology & Pathophysiology
Most often caused by the fungus Candida albicans (80%–92%), which is a normal part of the vaginal flora
Not necessarily associated with ↓Lactobacillus
↑ Estrogen levels → ↑ vaginal glycogen → favorable environment forCandidagrowth and adherence
candida BV
Clinical Presentation
Vulvar and vaginal
Pruritis, burning, and irritation
Erythema andedema
Vaginal discharge
Thick, white, curd-like
No odor
Dyspareunia
candida BV
Dx
Vaginal pH is normal
Wet mount with 10% KOH
Buddingyeast
Pseudohyphae
↑ WBCs
Clumps of epithelial cells
Negative “whiff” test
Vaginal culture (yeast)
When microscopy is unrevealing
Continued symptoms despite treatment
Trichomoniasis
General
Most common non-viralsexually transmitted infection (~2.6 million cases yearly)
Causative agent
Trichomonas vaginalis
Flagellated protozoan
Frequently coexists with BV
Often associated with other STIs and can enhance transmission of HIV
Associated with adverse obstetric outcomes
Premature rupture of the membranes
Preterm delivery
Delivery of a low-birth weight infant
Risk factors
Unprotectedsex
Multiplesexpartners
trich
♀ Clinical Features
Acute infection
Vaginal discharge
Frothy yellow-green discharge
Scant to copious
Malodorous (fishy)
Vaginal pruritus and irritation
Dysuria
Dyspareunia
“Strawberry” redcervix and red “strawberry” spots on the vaginal walls
Postcoital bleeding may also occur
Chronic infection
Signs and symptoms as above, but milder
Pruritus and dyspareunia with scant vaginal secretions
Trich
♂ Clinical Features
> 75% of cases are asymptomatic and transient (spontaneous resolution within 10 days)Symptoms
Clear or mucopurulent urethral discharge
Dysuria
Urge to urinate frequently
Burning or pruritus in the penis after sexual intercourse
