Assessment 6 Flashcards
Location and time of fertilization
Usually in ampulla of uterine tubes
Within 24hrs of ovulation
Time of implantation
Day 20-24 of menstrual cycle
3 weeks gestation
hCG
Human chorionic gonadotropin
Secreted by syncytiotrophoblasts
Bind LH receptors and promote progesterone secretion from corpus luteum
Detectable 9-11 days after LH surge
hCG other effects
Stimulates testes to secrete testosterone from Leydig cells (just like LH)
Promotes differentiation of cytotrophoblasts to syncytiotrophoblasts
Increase thyroid activity
Corpus Luteum secretion
Progesterone
17 hydroxyprogesterone - marker of corpus luteum b/c placenta cannot produce
Relaxin
Estradiol
hCG secretion change
hCG doubles every 2 days until peak @ 10 weeks
Pregnancy symptoms
Amenorrhea Vaginal bleeding/spotting Nausea w or w/out vomiting Elevation of temperature Fatigue Breast enlargement Increased urination with no dysuria
Pregnancy symptoms that are concering
Heavy bleeding
Nausea/vomiting after 10weeks gestation
Lightheadedness w/abnormal HR and rhythm
Dyspnea and other pulmonary symptoms
hPL and hPGH
hPlacental Lactogen: Secreted throughout, higher levels than hPGH
hPlacental Growth Hormone: Secreted later in gestation, shuts down maternal GH
Hormone involved with maternal insulin
hPL - decrease maternal insulin sensitivity
Increases lipolysis, decrease glucose uptake, increase gluconeogenesis
Glucose homeostasis in mother and fetus
Maternal: Insulin insensitivity, mobilize more free glucose for fetal use. fasting hypoglycemia, post prandial hyperglycemia, hyperinsulinemia
Fetus: Take glucose from mother
HPAdrenal Axis changes in pregnancy
Placenta produces CRH
Maternal hypercortisolism - Cushings levels, but progesterone can prevent other cushings symptoms
Fetus protected from high cortisol levels because of 11BHSD2: Cortisol –> Cortisone
Placental CRH difference from maternal
Cortisol has positive feedback on pCRH
Near term HPA axis change
Positive feedback from Cortisol increases - started by drop in CRH-BP
Less 11BHSD2 = increased fetal exposure to cortisol: Necessary for lung development and surfactant synthesis
Preterm labor steroids
Dexamethasone or betamethasone for babies born 23-34 weeks - hydrocortisone metabolized by 11BHSD2
Greater than 34 weeks not necessary
Less than 23 weeks lungs not developed enough for drug to work
Estriol
Major estrogen in pregnancy
Comes from 16a hydroxyDHEA-S in fetus liver
Travel to placenta and converted to estriol
Maternal-Placental-Fetal Unit
Placenta cannot make cholesterol - taken from mother
Placenta cannot make androgens (DHEA)
Fetus cannot make estrogens from androgens
Fetus and mom supply placenta with DHEA which gets converted to Estrogens
Progesterone functions during pregnancy
Increased secretions to nourish pregnancy
Decrease uterine contractility
Breast development
Alters cardiac and pulmonary parameters
Suppress immune function so fetus not rejected
Estrogen pregnancy functions
Increased uterine blood flow
Breast enlargement and ductal growth
Sink for weak androgens produced by fetus
Estrogen during labor
Increase uterine contraction and release of placental prostaglandins
Stimulates proteolytic enzymes in cervix for cervical dilation
Pregnancy and pituitary gland
Enlarges but no increase in blood flow
Hyperprolactinemia
Prolactin and pregnancy
Increase
Promotes alveolargenesis in breast
Milk synthesis post partum
Thyroid and pregnancy
Increase in TBG
Stimulation of TSHr by hCG
-Decrease TSH with increase FT4
Euthyroid hyperthyroxinemia
Pregnancy and renin angiotensin system
Increase in total body water
Estrogen drives activation of R-A-A system
Normal weight gain in pregnancy
25-35lbs
~22lbs gets lost after pregnancy
2/3 weight gain occurs in last 1/2 of pregnancy
Obesity and pregnancy
Increased risk of miscarriage, GD, preeclampsia, congenital defects, Csection
15lbs weight gain if BMI>30
Cardiovascular changes in pregnancy
Improve oxygenation and nutrient flow to fetus
Increase SV and HR
Decrease PVR = decrease in BP
Decreased vascular resistance mechanism
Progesterone and NO mediated smooth muscle relaxation
BP lowered
Maternal position and CVSystem
Sleeping on back can compress IVC and decrease SV and BP
Decrease uterine perfusion as well
GI and pregnancy
Increase appetite
Increase reflux - decrease LES tone
Nausea and vomiting - week 4-8 until 14-16. Increase hCG = stomach muscle relaxation
Decrease GI motility - decrease in motilin
Hemorrhoids
Cholestasis - empties slower (progesteron)
LDL increase, hemodilution, increase ALP
REnal changes in pregnancy
Ureter compression
Bladder loses tone (Progesterone), also compressed by uterus
Breast changes
Size increase
Ductal growth
Everything gets bigger/more pronounced
Delivery and breastfeeding
Decrease in hormones (prog, estrogen etc) removes feedback inhibition on PRL so milk synthesis can occur
Suckling
Oxytocin release
Contraction of myoepithelial cells in breast
PRL release
Ectopic pregnancy
Implantation not in uterus, usually in fallopian tubes
1/150 pregnancies
Ectopic pregnancy risk factors
PID Endometriosis Surgery Smoking IUD Age
Ectopic pregnancy symptoms
Late menses
Pelvic pain
Vaginal bleeding
Placental abruption
Placenta breaking off from uterus
Concealed bleeding or visible bleeding
Irritation from blood = uterine contraction = further breaking of placenta = more blood
Placental abruption risk factors
Smoking Trauma HTN pre-eclampsia Cocaine
Placental abruption grading
Based on amount of bleeding, severity of contractions, fetal distress/HR, BP, ab pain
Grade I, II, III (most severe)
Intrauterine growth restriction
IUGR = EFW less than 10%
Maternal HTN, smoking, cocaine, diabetes, renal disease, autoimmune, malabsorption
Macrosomia
EFW greater than 4000-4500g in diabetic pregnancy
EFW greater than 5000 in non diabetic
Diabetes in pregnancy
Due to insulin insensitivity caused by hPL
Decrease glucose uptake, increase lipolysis, increase gluconeogenesis
White classification
Takes into account duration/cause and if any end organs are involved
F - nephropathy
R - Retinopathy
H - CAD
T - transplant
Diabetic screening in pregnancy
- history at first visit
- Physical exam
- Glucola (1hr) test @ 240=-28 weeks
- Glucose tolerance test (if glucola is positive), 3hr test
Diabetic management with pregnancy
Patient education on diet
Glucose monitoring
Test for end organ damage
Fetal growth monitoring
Total amniotic fluid
500-1000mL
Replaced every 3hrs
Primarily from renal excretion
Oligohydraminos: Definition, cause, management
Not enough amniotic fluid - AFI less than 5
Causes: Rupture, placental insufficiency, fetal renal anomalies
Management: Inpatient care, rehydration, delivery at term
Polyhydraminos
AFI > 24
Causes: Maternal diabets, idiopathic, abnormal fetal swallowing, GI malformation (duodenal atresia)
Management: Fetal testing, delivery at term
7x increase of IUFD over Oligo
Hypertension and pregnancy incidence
Affect up to 10% of all pregnancies
Gestational HTN: 6-18% nulliparous, 6-8% multiparous
Pre-eclampsia: 3-5% nulliparous, .8-5% multiparous
Distinguishable features of pre-eclampsia compared to Gestational HTN
Occurs >20 weeks
Variable HTN
Proteinuria Increased Uric acid Hemoconcentration Thrombocytopenia (severe case) Hepatic dysfunction (severe case)
Pre-eclampsia classification: Mild
BP > 140 sys, >90 diastolic
Proteinuria
Protein/creatinine >.3
Pre-eclampsia classification: severe
BP > 160 sys, >110 diastol
Oliguria Visual disturbances Epigastric pain Edema HELLP IUGR Eclampsia (seizures)
Gestational hypertension
Most cases occur late, after 37 weeks
Increased progression to pre-eclampsia if diagnosis is remote from term
Delivery at term
Potential etiologies of Pre-eclampsia
Abnormal trophoblastic invasion
Coagulation abnormalities
Vascular endothelial damage
Immune issue
Genetics
Dietary deficiency
Normal vs pre-eclampsia pregnancy prostacyclin and thromboxane
Normal pregnancy: Prostacylin and thromboxane in balance
Pre-eclampsia: Shift towards thromboxane - Vasoconstriction, platelet aggregation, uterine activity increase, decrease uteroplacental blood flow
Pre-eclampsia risk factors
Nulliparous Fam Hx or previous Hx Obesity Multifetal gestation Molar pregnancy
Preexisting medical conditions
Preexisting thrombophilias
Complications of severe pre eclampsia by organ system
Cardiovascular: Severe HTN, pulmonary edema
Renal: Oliguria, renal failure
Neurologic: Cerebral edema, eclampsia (seizures), hemorrhage, amaurosis
Hepatic: Hepatic dysfunction and subscapular hematoma
Hematology: Hemolysis, DIC, thrombocytopenia
Uteroplacental: Abruption, IUFD, fetal distress, IUGR
HELLP Syndrome
Hemolysis
Elevated Liver enzymes
Low Platelets
Pre eclampsia Diagnosis
Identify risk first
Assess symptoms
BP monitoring
Proteinuria
Weight gain/edema assessment
Pre eclampsia management
Continuous fetal and uterine monitoring
Anesthesia
Antihypertensives
Delivery - base on severity
Recommendation for exclusive breast feeding?
First 6 months
Recommendation for breastfeeding + complimentary foods
At least 1 year old
No breast feeding increases risk of…
Acute otitis media (2 fold)
Gastroenteritis (3 fold)
Lower respiratory tract infection (3 fold)
SIDS (50%)
Necrotizing enterocolitis (1.5 fold)
Only formula increases risk for…
Atopic dermatitis
Asthma
Obesity
Diabetes
Leukemias
Breast milk contents
Immunoglobulins Cytokines Growth factors Anti microbial Metabolic hormones Oligosaccharides (anti infection) Mucins (infection block)
Breast milk supply and demand
Increase supply by adherence to breast feeding
No skipping/milk substitutes
Milk production stages
Lactogenesis I, II, III
Lactogenesis I
Secretory differentiation
Preparation of mammary gland to make milk
Mid pregnancy, increased prolactin
Lactocytes differentiate
Colostrum
First milk
Lactogenesis II
Secretory activation
Onset of copious milk production
Triggered by expulsion of placenta, decrease in hormones removes PRL inhibition
Lactose activates, water drawn into lactocyte
Increase from 20-30mL to 500+mL week 1 post partum
Lactogenesis III
Maintenance of milk output
Production dependent on continual removal, less on hormones
Oxytocin and lactation
Secretion stimulated by suckling, baby smell/sound
Milk ejection via myoepithelial cell contraction
Common breast feeding problems
Milk supply issue
Difficulty feeding
Solutions for breast feeding issues?
Baby friendly hospitals
Steps for successful feeding
Peer and professional support post partum
Benefits of scrotum
Thermoregulation
Sperm fitness
Social signal
Clitoral stimulation?
Spermatic cord contents
Pampiniform plexus
Cremaster muscle
Testicular artery
Vas deferens
Genitofemoral nerve
Thermoregulation of testis - pampiniform plexus
Counter current between plexus and testicular artery
Heat from body blood transferred to venous plexus blood traveling back to body leaving testes blood cooler
Varicoceles
10% men affected
Abnormal dilation of veins in spermatic cord
Palpable/enlarged vein, atrophy, lower testosterone levels
Varicocele cause
Idiopathic - incompetent valves
Secondary - compression of venous drainage: nutcracker, pelvic/abdominal malignancy
Left sided varicoceles?
Left testicular vein drains into left renal vein instead of larger IVC
Dartos fascia
First layer under skin
Smooth muscle components contract and relax testes to bring closer or move further from body
Cremaster muscle
Arise from internal abdominal oblique
Lowers and raises testes to regulate temperature
Brings testes closer to body during running/fighting/stress
Cremasteric reflex
Cremaster muscle innervated by genital branch of genitofemoral nerve (L1/L2)
Inner thigh stimulation induces cremaster contraction
Spermiogenesis
Process where spermatids become mature spermatozoa
Development of middle piece/tail
Formation of acrosome
Sertoli cell
Epithelial cell of seminiferous
AMH secretion
Inhibin and activin secretion
Androgen binding protein to increase testosterone accumulation
Establish blood testes barrier
Glial cell line derived neutrophic factor
Produced by sertoli cell
Spermatogonia self renewal during perinatal period
ERM transcription factor
Produced by sertoli cell
Maintenance of spermatogonial stem cells in adults
Spermatogenesis and 2 cell theory
LH binds to Leydig cell and induces androgen synthesis which travel to Sertoli cell and bind to receptors in nuclei
FSH binds to Sertoli cell and weakly stimulates spermatogenesis
Presence of BOTH FSH and Androgens = strong stimulus for spermatogenesis
Sertoli cell only syndrome
Germ cell aplasia
Only sertoli cells present
Infertility, azoospermic
Deletions in AZF region of Y chromosome
Exogenous androgen
Exogenous androgen exerts inhibitory effect on pituitary gland –> Decrease LH –> Decrease in spermatogenesis
Path of sperm
Seminiferous tubules –> Straight Tubules –> Rete Testis –> Epididymis –> Vas deferens –> Ejaculatory Duct –> Urethra –> Penis
Testicular cancer risk factor
Cryptorchidism
Previous testicular cancer
Previous male infertility
Family history
Downs
Orchitis
Inflammation of testes
Blood in sperm/urine, sever pain, swelling
Causes: STD, mumps, ischemia
Treatment: Oral antibiotics, NSAIDS
BPH
Benign prostatic Hyperplasia
Plastic growth of prostate gland
Polyuria, urgency, nocturia, hesitancy
Enlarged prostate on digital rectal exam
BPH surgery
Transurethral Resection of Prostate Gland
Pharma options for BPH
Alpha 1 adrenergic antagonists
5a reductase inhibitors
Alpha 1 adrenergic antagonists
Prazosin, Doxazosin, Tamsulosin
Antagonize alpha 1 receptors, inhibit bladder smooth muscle contraction
Can also affect vascular smooth muscle - risk of orthostatic hypotension, nasal congestion, reflex tachycardia
Tamsulosin benefit
Tamsulosin is specific for bladder alpha 1 receptors
Less likely to cause hypotension and dizziness
5 alpha reductase inhibitor
Prevent production of DHT which can limit plastic growth of prostate gland
Finasteride, dutasteride
Sexual dysfunction, ED
Can lower PSA so may hide other issues such as malignancy
Bulbourethral gland
Cowpers gland
Secrete salty mucous secretion
Lubricates urethra, neutralize acidity
Parts of urethra
Spongy, membranous, prostatic
Bladder blood supply
Internal iliac artery supplies bladder - Superior and inferior vesicle arteries
Venous return to vesical and prostatic venous plexus
Bladder innervation
Internal sphincter - parasympathetic from pelvic splanchnic nerves
External sphincter - somatic from pudendal nerve (perineal nerve deep branch)
Balantis
Inflammation of glans peins
Bacteria, irritation, HPV, diabetes
Antibiotics/antifungal, hygeine
Phimosis
Foreskin too tight and cant be pulled back
Congenital, injury, inflammation
Treat with steroid creams or circumcision
Rupture of penile urethra but not Buck’s fascia
Swelling contained to penis only
Rupture of penile urethra and Buck’s fascia
Collection of liquid deep to Colle’s fascia
Lower abdominal wall, testes
Superficial pouch
Prostomembranous junction rupture of urethra
Retroperitoneal hematoma and urine extravasation
Limited to deep perineal pouch
Peyronie’s diseas
Connective tissue disorder
Scar tissue in tunica albuginea
Pain, abnormal curvature
Trauma/injury
Penis blood supply
Internal pudendal artery from internal iliac
Penis innervation
Somatic nerve supply from pudendal nerve
Dorsal nerve of penis
Detailed penis vasculature
Pudendal artery –> Dorsal and deep artery of penis –> Helicine arteries –> Sinusoids –> Emissary veins –> Circumflex veins –> Deep dorsal vein –>
Flaccid vs erectile state of penis
Flaccid: Lacunar space compressed and sufficient venous outflow
Erectile: Dilation of lacunar space (trabeculae SM), blood inflow increase and venous compression (decreased outflow)
Erection and nervous system
Sensory or touch stimulus to penis –> Dorsal nerve of penis –> S2-4
Pelvic splanchnic parasympathetic nerves dilate erectile tissue arteries
Secretion
Release of fluids from seminal vesicle, prostate, bulbourethral glands
Cholinergic axons from inferior hypogastric plexus
Emission
Movement of ejaculate into prostatic urethra
Postganglionic sympathetic neurons of inferior hypogastric plexus
Peristaltic contractions of epididymis and vas deferens
SM contraction of prostate and seminal vesicle
Internal urethral sphincter contraction prevents retrograde ejaculation
Ejaculation
Release of ejaculate from penile urethra
Pudendal nerve fibers cause contractions of bulbospongiosus muscle
Synonymous with orgasm
Detumescence
Cessation of sexual stimulus
Vasoconstriction of arteries, trabecular contraction, loss of blood filling erectile tissue
Normal signaling pathway for erection vs ED
Normal: Stimulus –> NO increase –> Guanylyl cyclase increase –> cGMP formation –> smooth muscle relaxation –> increase blood flow
ED: cGMP converted to inactive GMP –> no SM relaxation and erection
Phosphodiesterase 5 inhibitors
PDE-5 inhibitors
Sildenafil (Viagra)
Vardenafil (Levitra)
Tadalafil (Cialis) - long lasting
Avanafil (Stendra) - absorbed quickly
PDE 5 inhibitor interactions
Metabolized by CYP3A4
Transiently lowers BP
Don’t use organic nitrates for angina
PDE 5 inhibitor selectivity
Sildenafil and Vardenafil inhibit retinal PDE5 - blue eyes
PDE1 in vascular smooth muscle inhibited by sildenafil and varendafil - vasodilation, tachycardia, flushing
Steps of viral infection
Attachment Penetration Uncoating Biosynthesis Assembly Release
HPV: Structure, pathogenesis, diagnosis, prevention/treatment
Structure: Circular DNA genome, no capsid
Pathogenesis: Direct contact. Replication basal cell nuclei of epithelium, no systemic spread. Transform wart–>carcinomas
Diagnosis: Cytology, immunohistochemistry, nucleic acid
P/T: Vaccine, Pap smear, surgery
Herpes simplex virus
Can be latent or active
Virus present in axons
Virion protein 16 acts with HCF
VP16 transcription factor not transported to neuronal nuclei = latency
VP16 promoter promotes prduction of VP16 which initiates replication and end of latency
Complete hydatidiform mole
Total lack of fetus but placenta present and growing
Enlarges because continually absorbing fluid
Uterine enlargement, first trimester bleeding, second trimester pre-eclampsia
Elevated hCG
Large avascular chorionic villi, trophoblastic atypical proliferation
Complete hydatidiform mole genetics
Two sets of paternal chromosomes, empty egg
p57 gene (paternally imprinted): Tumor suppressor and cell cycle inhibitor
No maternal gene to express
p57 negative
Partial hydatidiform mole
Variable uterus size
Variable hCG
Fetus MAY be present, usually abnormal
Two populations of chorionic villi: Large avascular villi with convoluted outlines and small vascularized villi
Partial hydatidiform mole genetics
Triploid and diandric: Two paternal, one maternal
p57 expressed (maternal chromosomes)
Invasive mole
Hydatidiform mole that penetrates uterine wall
Persistent elevation of hCG after curettage
Responds to chemo
Can cause uterine rupture
Choriocarcinoma
Malignant neoplasm with atypical trophoblasts, no chorionic villi
Biphasic tumor (cyto and syncytiotrophoblasts
LARGE amounts of hCG
Acute chorioamnionitis
Cloudy membrane, smelly amniotic fluid
Premature rupture of membrane and premature labor
Most common cause of death in 2nd trimester
Placental membrane inflammation - neutrophils
Acute subchorionitis
Maternal response to amniotic sac infection
Leukotactic signal
Neutrophilic infiltration of subchorionic fibrin
Chorionic plate vasculitis
Fetal inflammatory response
Severe ascending infection
Polymorphonuclear leukocytes migrating from fetal blood
Umbilical cord vasculitis and funisitis
Fetal inflammatory response
Umbilical cord compression
Polys of fetal origin
Intrauterine pneumonia
Poly leukocytes in terminal air spaces
Usually lethal
TORCH infection
Toxoplasmosis Other (Syphilis) Rubella CMV Herpes
TORCH clinical features
Fetal growth restriction BRain lesions Eye lesions Hepatosplenomegaly Skin lesions
Listeriosis
Placental inflammation, stillbirth, neonatal sepsis
Abscess formation in lungs, liver, lymph nodes
Most common fetal virus
CMV
Oligohydraminos causes
Renal agenesis/malformation
Urethral obstruction
Chronic leakage of amniotic fluid
Decreased production or increased absorption of amniotic fluid
Oligohydraminos clinical presentation
Amnion nodosum
Fetal compression - Potter’s face, abnormal limbs, Breech
Pulmonary hypoplasia - Respiratory insufficiency and death
Amniotic band syndrome
Disruptions and deformations caused by amniotic bands
Craniofacial, abdominal wall defects
Monosomy X
99% die in utero
Generalized edema, cystic hygroma, aortic coarctation, bicuspid aortic valve
Trisomy 21 prenatal screening
Quintuple test: 2nd trimester maternal screen -
hCG - High
Urinary Estriol - Low
AFP - Low
Inhibin A - High
Pregnancy associated plasma protein A - Low
Trisomy 13
Pateau syndrome
1:5000
No separation of cerebral hemispheres Cleft lip/palate Omphalocele Renal anomalies Cardiac malformations
Trisomy 18
1: 8000
Less than 5% survive to term
Quintuple test: All 5 components low
Polyhydraminos, globular head, low set ears, cardiac malformations, overlapping fingers
Thanatophoric dysplasia
Most common lethal dwarfism
Gain of function mutation in FGFR3 - different than achondroplasia
Micromelic limb shortening, telephone receiver femora, large head, narrow thorax
Disorganization and retardation of bone growth plates
Osteogenesis imperfecta
Autosomal mutation in genes for alpha 1 and alpha 2 collagen chains
Deficiency in type 1 collagen synthesis
Most common connective tissue inherited disorder
Four subtypes
Most severe: Type II - intrauterine fractures, blue sclerae, thin calvarium
Environmental causes of congential anomalies
TORCH infection
Maternal diabetes
Drugs/chemicals: FAS, Retionic acid, Thalidomide
Diabetes embryopathy/fetopathy
Cardiac anomalies, neural tube defects, caudal regression syndrome - Embryopathy
Fetal macrosomia due to maternal hyperglycemia induced fetal - fetopathy
Neural tube defects
Environment and genetic
Folate deficiency and hyperthermia during early gestation
Diagnosis: Very elevated AFP
Confirm with ultrasound
Signs and symptoms of fetal hypoxia
Abnormal fetal movements
Passage of meconium
Abnormal fetal HR
Abnormal fetal blood sampling
Fetal hypoxia pathogenesis
Reduced placental perfusion –> Increase stress and decrease fetal oxygenation –> CO2 accumulation and metabolic acidosis
Acidosis = impaired cardiac function
Severe birth asphyxia = brain damage, can lead to death
Fetal hydrops causes
Intrauterine heart failure Chromosomal anomalies (Turners, Tri 18/21) Structural abnormalities that interfere with circulation Chronic anemia = cardiac failure
Chronic anemia and hydrops
Parvovirus B19 transplacental infection
Infect erthyroid precursor, inhibit red cell maturation
Immune hydrops: Rh
Chlamydia life cycle
Elementary body: Hard, small, extracellular, infectious
Reticulate: Large, intracellular, replicative
Chlamydia serovar D-K
Urethritis, PID
Co infection with gonorrhea
Less acute manifestations, more chronic sequelae
Chlamydia Serovar L 1-3
Lymphogranuloma venereum
Sex organs–> inguinal lymph nodes and abscess formation
Rectal infection –> proctocolitis
Chlamydia diagnosis
Nucleic acid amplification tests
Sensitivity >90%
Chlamydia Treatment
Azithromycin PO once
Doxycycline 100mg BID 7x a day
Only test for cure in pregnant women
Gonorrhea
G(-) diplococcus
Multi drug resistant
Hard to grow - oxidase positive, CO2
Gonorrhea transmission
Guys more likely give to girl
Short incubation
No lasting immunity
Gonorrhea virulence factor
Pili - adherence to host tissue, multiple genes to avoid antibody binding, antigenic variation as well
Opa proteins - Surface proteins, bind to neutrophils and T/B cells
Gonorrhea antigenic variation
Change pili AA sequence to adhere to host tissue
High frequency changes
Can avoid immune response
Gonorrhea lipooligosaccharide
Outer membrane of G(-) - LPS
Hide from Ab
Membrane rupture of organism = Lipid A activation = immune activation and tissue damage
Also TNF-alpha release
Gonorrhea testing
Nucleic acid amplification test
Culture - resistance
Gram stain of urethral specimen
Gonorrhea treatment
Ceftriaxone shot x1
Azithromycin x1
Test cure if alternate regimen is used
Syphilis
Cant be cultured or seen on gram stain
Dark field microscopy or fluorescence
Human reservoir only
Painless chancre at site of disease - primary
Secondary - Systemic disease after untreated primary - rash/fever/lymphadenopathy
Tertiary - CNS involvement
Latent syphilis
Early - within year acquisition
Late - Over a year ago/unknown acquisition
NO SYMPTOMS
Syphilis diagnosis
Serologic test:
Non treponemal (RPR, VDRL) - antibodies directed against indirect signs of active synthesis
Treponemal (FTA-ABS, TP-PAA) - Antibodies against specific antigens on bacterial surface
Positive for life
Syphilis treatment
Penicillin always
Haemophilus ducreyi
Causative agent of chancroid
Gram (-)
School of fish appearance
Painful ulcer and lymphadenopathy
Leuprolide: MoA, Use
GnRH agonist
Prostate cancer, central precocious puberty, endometriosis
Gosrelin
GnRH agonist
Prostate cancer
Flutamide
Inhibits androgen uptake/binding to target tissues
Hepatic toxicity
Clomiphene and Te
Partial agonist to Estrogen receptor (acts as antagonist)
Increase Te production and spermatogenesis by blocking negative E feedback on Leydig cell
Hypogonadism diagnosis
Low 8am Te concentration on 3 separate occasions
7 Cardinal movements of Labor
- Engagement - Head moves to level of ischial spine
- Descent - Fetus moves towards pelvic inlet
- Flexion - Head reaches pelvic floor, bends forward onto chest (smallest anteroposterior diameter)
- Internal rotation - Head rotates, enters pelvic inlet
- Extension - Internal rotation complete, head exits
- External rotation - Body rotates so shoulders can fit
- Restitution/expulsion - Anterior then posterior shoulder exits
Definition of true labor
Contractions at regular intervals
Interval shortens
Intensity increases
Duration of contraction increases
Progressive cervical dilation and effacement
Not stopped by sedation
3 P’s of labor
Power
Passage
Passenger
Fetal lie types
Longitudinal
Transverse (Can’t be delivered)
Oblique
Stages of Labor
First stage: Initial onset of true labor pains to complete cervical dilation
Second stage: Complete cervical dilation to birth of baby - Pelvic and perineal phases
Third stage: Delivery of placenta
Fourth stage: Contraction and retraction of uterus
Prostatitis
Infection of prostate
Perineal or back pain
Acute bacterial - fever/chills/dysuria
Chronic bacterial - Hard to treat
Prostatic Intraepithelial neoplasia
Precursor lesion to prostatic carcinoma
Basal cells present. Superficial cells show nuclear enlargement and prominent nucleoli
Base grade on atypia
Prostate adenocarcinoma
Most common male cancer, 2nd leading cause of cancer death
Grading and staging important
TNM - T = How far tumor has moved
N = lymph node
M = distant metastases
Travel to bone
Testicular Lipoma
Proximal spermatic cord
Testicular adeomatoid tumor
Upper pole of epididymis
Rhabdomyosarcoma
Distal end of spermatic cord
Types of Testicular tumors
Germ Cell
Mixed Germ Cell
Sex Cord Stromal
Germ Cell Tumors
Seminomatous
Non seminoma
Seminoma tumors
Seminoma
Spermatocytic seminoma
Pathogenesis of germ cell tumors
Most originate from intratubular germ cell neoplasias
Cryptochordism, genetics, tetses dysgenesis are all predisposing factors
Seminoma
Large polyhedral clear cytoplasm
20-40yo
Spermatocytic seminoma
Males over 65
3 types: Small, medium, giant
Rarely metastasize
Non seminoma tumors
Embryonal carcinoma
Yolk Sac
Mature/immature teratoma
Choriocarcinoma
Embryonal carcinoma
20-30yrs
Only 3% aggressive
Many mitotic figures
Yolk Sac tumor
Elevated AFp
Schiller Duval bodies
Most common testicular tumor before age 3
Testicular Choriocarcinoma
1% of testicular tumors
Aggressive
Beta hCG
Mixed germ cell tumors
Have components from multiple individual germ cell tumors
Leydig cell tumor
Rare, 2%
Crystalloids of Reinke
Majority benign
Sertoli cell tumor
Rare
Cord like structures form
Majority benign
Staging of germ cell testicular tumor
Stage I - Confined to testis
Stage II - Spread to lymph nodes below diaphragm
Stage 3 - Metastasized above diaphragm or to other lymph nodes
Condyloma Acuminatum
HPV 6/11
Papillary excrescences
Bowen’s disease
Solitary plaque on shaft or scrotum
Atypical cells
Bowenoid papulosis
Verrucous carcinoma
Invasive carcinoma
Rare nodal involvement or metastasis
