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131 Cards in this Set

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*Physiologic Tremor
-predominantly in the hands
-increased w/ epi and adrenergic stimulants
-DEC w/ ETOH and B-adrenergic blocking agents
Cerebellar Tremor
-intention, ataxic, rubral
-occurs at the end of a purposeful movement
***Parkinson's Tremor
-resting tremor that disappears w/ action
-frequency 3-5 hz
-"pill rolling"
-increased w/ stress
-decreased w/ Dopaminergic agents
***Essential (Familial, Senile)
-predominantly in hands, but can be in head "yes-yes" or "no - no" motion*** and also can be in vocal cords
-increased by anxiety, B-adrenergics, and xanthines
-decreased by ETOH, propanolol, and primidone
-evident w/ arms outstretched (postural tremor) and also on finger nose finger testing (action tremor)
***Head tremor is seen in ________ but NOT _____?
-Essential tremors but NOT Parkinson's disease
What are treatments for Essential Tremor?
-Propranolol - most effective B-blocker: decreases amplitude of tremor
-primidone
-gabapentin, benzodiazepenes, pregabalin may also help
-DBS of thalmus
***Parkinson Tremor vs Essential tremor

1. Parkinson's Tremor
-initial sx in 70% of PD pts
-resting tremor that disappears w/ action
-rhythmic "pill-rolling" movement of thumb and index finger
-intermittent
-postural tremor occurs w/ hands outstretched? (I though this was essential????)
***Parkinson Tremor vs Essential tremor

2. Essential
-often starts 30-40's
-action induced tremor which lessens or disappears w/ rest
-mild asymmetry, arms usually first -> head, neck, jaw, and voice may all become involved
-often disabling (impairs fine motor skills)
*Chorea
-abnormal involuntary movement disorder
Athetosis
-continuous stream of slow, sinuous, writhing movements
Ballismus
-violent involuntary rapid and irregular movements
Dystonia
-sustained muscle contractions which cause twisting and repetitive movements or abnormal postures
***Asterixis
-tremor of the wrist when the wrist is extended (flapping tremor)
***Primary Torsion Dystonia (aka Dystonia musculorum deformans)
-disinhibition and facilitation of thalamocortical circuits
-childhood/adolescent onset focal or regional dystonia evolving into generalized truncal dystonia
-R/O Wilson's disease and Dopa responsive dystonia
-tx: anticholinergic, antidopaminergic, Botox (very effective for FOCAL dystonia), DBS of Globus palidus
***Wilson's Disease
-AR, abnormality in the enzyme ATP7B leads to impaired copper metab
-ceruloplasmin is decreased --> Cu deposits in tissues (liver, brain, iris)
-Kayser-fleisher ring (perimeter of iris Cu deposition)
What are the labs for Wilson's
-Dec ceruloplasmin
-increased serum copper
-increased urinary copper
-liver biopsy shows copper deposition (usually liver presents earlier)
What are some of the neuro-pyschiatric sx?
-mild cog impairment, clumsiness, ataxia, tremor, parkinsonism, depression...etc
***What is the tx of Wilson's
-chelation using agents which bind Cu and remove Cu deposits (penicillamine)
-Trientene hydrochloride is the DOC
***Huntington's disease
-30-50 yo onset, death ~15 yrs
-death from advance dementia
-choreic movements: continuous, abrupt, rapid, brief, unsustained irreg movements dance like gait
-milkmaids grip: when attempting to grip object, they alternately squeeze and release
-serpentine tongue
-psych sx before movemnt disorders
***HD is a true _____
-Auto Dominant disorder (homozygotes and heterozygotes do not differ clinically)
-HD gene is on short arm of chromo 4, abnL gene contains extra copies of CAG repeats (37-86)
-higher the repeats, worse the HD
*Juvenile HD
-under 20
-progressive parkinsonism, ataxia, dementia, and seizures
-80 repeats of CAG likely juvenile HD
-L-Dopa for parkinsonism in Juvenile HD
Tx of HD
-benzodiazpines for anxiety
-antidepressants and antipyschotics
***CT/MRI will show?
-loss of volume of caudate nucleus and putamen
-PET will show decreased flouro deoxy glucose metab in striatum
***Acute dystonic rxns may occur w/?
-Antiemetics - REGLAN
***Akathisia
-inability to remain in a sitting position
-motor restlessness and feeling of muscular quivering (not seen)
***Tardive Dyskinesia
-bucal, lingual, masticatory dyskinetic movements common
-MC appears w/in 3 months of withdrawal from DOPAMINE BLOCKERS (neuroleptics, reglan)
***What are the 4 cardinal signs of parkinsonism?
TRAP (need 2 of 4)
-Tremor (resting)
-Rigidity (cogwheel)
-Akinesia (bradykinesia is the hallmark feature of early PD)
-Postural impairment (forward tilt of trunk b/c of tendency to fall backwards)
*Rigidity of PD
-increase in muscle tone best tested at wrist, elbow, or neck
-cogwheel/rachet - like character when muscle tone is tested
*Akinesia
-masked faces
-difficulty initiating movement
-decreased blinking and swallowing
-decreased force of speech (hypophonia)
-difficulty rising from chairs or turning in bed
*Posture in PD
-retropulsive: tendency to fall back
-forward stoop
-unsteady-uncertain - in turning or on stairs
Early PD
-bradykinesia (hallmark)
-resting tremor in 80%
-asymmetry
-tremor dominant cases have good prognosis
-rigid-akinetic cases progress more rapidly
-NO postural or impaired balance
Later stage PD
-postural impairment (usually after 3-5 yrs)
-hesitation when initiating movement or freezing spells
-if postural impairment and falls occur in first year then prob ATYPICAL PARKINSONISM
*Atypical parkinsonism
1. Multiple system atrophy
2. Progressive supernuclear palsy (axial>limp rigidity, early balance problems)
3. Corticobasalic ganglionic degeneration (alien limb)
4. Secondary parkinsonism (stroke, tumor)
***Non motor sx of PD
-Dementia (lewy body in cerebral cortex)
-depression and anxiety
-olfactory dysfxn
-pain and sensory complaints
-ANS dysfxns (ortho hypotension, syncope, swallowing problems, urgency/incontinence, decreased libido, ED)
NYCOM study for PD
1. Tx group got OPP
2. Sham tx group ROM (not to endpoint were preformed on pts w/ PD
3. Control group - age matched pts w/out PD
What did the OMT tx for the PD pts consist of?
-lateral and AP translation of T and L vertebrae, OA release, active MFR of T and L vertebrae, cervical translation and ME, spencer techniques, etc
***Conclusions of the study
-stride length increase 8 cm (stat sig) in tx group
-cadence increased (not stat sig) in tx group
-upper limb velocity increased (shoulder swing stat sig and wrist movement NOT stat sig) in tx group
-lower limb velocity increased (hip stat sig; knee and ankle not stat sig) in tx group
**OPP and MS
-direct MFR and ME addresses spasticity
-cranial techniques: addresses balance and coordination
Case: 48 y/o G3P3 c/o 2 year hx of involuntary loss of urine 4-5x/day typically occurring IMMEDIATELY after coughing sneezing or heavy lifting. Occasional dysuria and a strong urge to void during these episodes. She is embarrassed, otherwise healthly. UA nL, slightly obese, BP 130/80, HR 80bp. Type of incontinence?
-MIXED (b/c she leaks w/ valsalva (sneeze/cough) and has a strong urge to void w/ dysuria
***Genuine Stress Incontinence
-hypermobility of the urethrovesicle junction d/t trauma (ex childbirth)
-involuntary loss of urine, NOT preceded by urgency
-anatomic defect is present (ex. increases in intra-abd pressure are exerted against the proximal urethra as well as against the bladder)
-MC in women < 75 yo
From handout:

What is the definition of incontinence?
-the involuntary loss of urine to a degree sever enough to have social and/or hygenic consequences
-affects 25% of repro age women, 50% of post meno women, and 75% of nursing home residents
From handout:

What is the psychosocial impact of incontinence?
-depression, embarrassment, decreased social interaction, a feeling of not winning, and decreased sexual activity
-becomes even worse should there be a failed surgical procedure
From handout:

*Any time the sum of the intra-abd pressure + ________ exceeds the _____ urine will come out
-bladder pressure exceeds the urethral closing pressure
From handout:

Physiology of voiding
-parasymp of ANS innervates detrusor muscle via sacral plexus
-stim --> contraction of detrusor and emptying of bladder
-SYMP division of ANS innervates bladder neck and INTERNAL sphincter thru alpha-adren receptors via hypogastric plexus
-Pudendal innervates EX sphinc and pelvic floor --> voluntary control
From handout:

***Most of the pt seen in primary care are either _____ incontinence or _______ or a combination of the 2
1. genuine (anatomical) stress incontinence [GUSI]
2. Detrusor instability (DI) [sometimes just called urge incontinenc)
or a combo of the 2
From handout:

****Why is it so important to distinguish GUSI from DI?
-GUSI is basically tx surgically: Trans-vaginal tape
-DI (aka urge incontinence) is tx medically via anticolinergics and oxybutin
***Urge incontinence
-"detrusor instability"
-loss of urine d/t an uninhibited and sudden bladder contraction (overcomes ones conscious input to hold urine)
From handout:

***Urge incontinence
-MC form in women >75
-DI is the cause of most urgency incontinence
-volume lost are large compared w/ stress incontinence
-loss may occur from any position
From handout:

*Coughing and incontinence:
DI vs GUSI
-although DI may occur after a cough, loss is DELAYED several seconds after the cough in contrast to GUSI in which case it occurs SIMUTANEOUSLY w/ the cough
***Overflow incontinence
-bladder no longer "Knows" its full and needs to empty which is nL conducted via afferent input to brain
-a/w overdistended hypotonic bladder in the ABSENCE of detrusor contractions
-2ndary to bladder neuropathies (DM and MS)
***How do you tx overflow incontinence?
-Tx w/ behavioral modification (pee schedule) bc neither surgery or medication will help
From handout:

Total incontinence
-abnormal drainage situations (ie fistulae, diverticulae, ectopic ureter)
****Reversible forms of incontinence:

DIAPPERS
-Delirium
-Infection
-Atrophic vagininitis
-Psychological
-Pharmacologic
-Excess fluid
-Restricted mobility
-Stool impaction
From handout: (and kinda from Noteservice)

-Why is it important to ALWAYS get a UA and culture from a pt w/ a c/o new onset urinary incontinence?
-UTI may cause urge incontinence
-definition of UTI >150,000 CFU
*Atrophic Vaginitis
-at menopause d/t lack of estrogen
-bladder is estrogen dependent (has lots of collagen)
-Tx: estrogen
*Pyschological
-when leak urine and stool when depressed
-tx SSRI, antidepressants
*Excess Fluid states
-DM, SIADH, periph edema, CHF
-tx: furosemide (diuretic)
*Restricted mobility
-ex in nursing homes
-tx: pt should be assisted to bedside commode every hour one the hour while awake
*Stool impaction
-decreases relative capacity of the bladder
-tx: disimpaction, enema
*Risks for incontinence
-obesity
-prego (especially w/ big babies b/c stretches the vesicoureteral junction)
From handout:

** a dx of GUSI is suggested by...
continence while lying down and spurts of urine SIMULTANEOUS w/ increases in intra abd pressure
From handout:

** a dx of DI is suggested by...
urgency, frequency, nocturia, enuresis and supine incontinence
From handout:

** a dx of OVERFLOW is suggested by...
-loss of small amounts of urine + frequent voiding of small amounts
From handout:

** a dx of ATROPHY is suggested by...
=hypoestrogenic states (ie menopause, lactation, oophorectomy)
***Why is limping in a child such a complicated issue?
-bc it can come from ANYWHERE!
-*hip pain often presents as knee pain
-kids arent good at localizing pain and don't complain if they arent using jt
-parent knows if kid is walking funny
-check out everything first before attributing pain/limp to trauma (examine involved jt last)
*DDx of Limp for ALL ages
-septic arthritis
-osteomyelitis
-stress fracture
-neoplasm
-marrow swelling (leukemia)
-neuromuscular (musc dystrophy)
***DDx of Limp for TODDLER
-developmental hip dysplasia
***DDx of Limp for 3-10 y/o
1. Legg-Calve-Perthes
2. Juvenile RA
3. Toxic synovitis
*DDx of Limp for adolescents
-slipped capital femoral epiphysis (essentially a femoral head fracture)
***Septic arthritis
-if not tx, need jt replacement
-often w/ fever
-*MC < 2 yo and >10 yo
-Staph is MCC
-Knee and hip is MC
-DX: joint aspiration w/ analysis of synovial fluid (turbid)
-Tx: ortho emergency (need jt drained) and Abx long term
***Toxic (Transient) synovitis
-***MCC of jt pain in kids 3-8
-Hip is MC
-follows viral infection by 1-2 weeks
-resolves in 2 days-2 weeks
-w/u is generally negative
***Care of limping child:

Febrile vs Afebrile
1. Febrile: Jt aspiration and culture
2. Afebrile: CBC, Sed rate or CRP, joint X-ray
*** if all nL = tx as transient synovitis but re-evaluate in 2 days if not better
*Case: 13 month M w/ 3 day hx of irritability and refusal to move left leg. Cold 2 w ago and intermittent. Fever 100.4F and is nontoxic although looks uncomfortable. Left leg flexed and externally rotated. CBC = WBC 24k (nL 12k) and left shift, CRP is 12 (nl .5), Hip asp = fluid thin & turbid, WBCs 3000, G+ cocci in clusters. How to tx?
-drain in OR
-Abx for weeks (if bone involvement requires 6 weeks of abx)
***Case 2: 12 y/o M w/ 6 day hx of left sided limp/ C/o pain in left thigh and knee. Denies fever, preceding illness and trauma and is otherwise good health. CBC normal, CRP unremarkable. What will X ray show?
-Slipped capital femoral epiphysis (SCFE)
-salter 1 fracture through the epiphyseal plate
-ORTHO emergency: put screws in there to re-align. [complication = avascular necrosis, deformity]***
-typically ion adoles obese males, d/t excess wt and shear stress
**Legg-Calve-Perthes
-degeneration disease of the head of femur
-rapid linear growth and blood supply just can't keep up so you get involution
-very serious condition
-tx is braces (don't immobilize too long)
*Case 3: 3 y/o M w/ limp this morning/ had an URI 1 week ago that resolved. Left hip pain. Labs normal. Dx?
-Toxic synovitis
-initial intervention is to tell parents child should have light activity and give NSAIDs, re-eval in 48 hrs
-if not better: bone scan (afebrile) or x-ray and aspiration (febrile)
*Case 4. 3 y/o M w/ 3 d hx of fever (101.8 F) and limp. All other vitals are nL. Antalgic (painful) gait favoring R leg. mild discomfort w/ passive movement of R hip only. WBC 56K, Lymphocytes 81%, Platelets very low, RBCs very low. LDH is 290 (very high). Work up and potential dx?
-W/U would be aspirate the hip and an Xray b/c pt is Febrile
-Dx: Leukemia (ALL): LDH is very high which means some abnL WBC activity, and 81% lymphocytes whereas after 2 y/o PMNs should predominate
Case 5: 6 y/o w/ fever of 101 F for 2 d. Limp on L side. CBC and CRP are high. X ray nL...
-in OR the SURGEON noticed an enlarged abdomen (I thought we were supposed to be dumb?)
-the pt had a psoas abscess (hence pain can be referred)
***Aproximately how many women suffer from cervical cancer in the USA and then in the rest of the world?
-only about 11k b/c of our pre-screenings
-world wide 500 k in part b/c of lack of screenings and also bc the HPV pandemic is devastating the rest of the world
*List or describe as many of the causes of cervical CA that you can?
-Immunocompromised, HPV
-STDs
-HIV, smoking, stress, chlamydia
-Risk factors: being slutty, early sexual encounter
-prog of cervical CA is ~10 years
-also note that early menarche could lead to ovary CA b/c more insults to the ovary
*List as dx tools that the average "run of the mill physician" might utilize to workup and dx of cervical cancer?
-hx and physical skills
-HPV DNA testing
-Laproscopy
-Pap
-biopsy
-vinegar w/ acetic acid (take up by cells affected by the virus and they turn bright white), colposcopy
-TVUS
-MUST DO A RECTAL
***Findings that may be found in cervical CA?
-increase mitotic features, blood, koilocytosis, finger like projections, hyperchromatin, loss of cell polarity
* List some of ways cervical CA may be tx in pts w/ diagnosis. Surgical and medical?
-Leap and cone
-Radical hysterectomy
-Wide excision
-chemo
* If surgery did not go well and pt looks like they are going into shock...
-fresh frozen plasma
-nL saline
-intubate

*this is a fucking stupid question
*What is a cold cone biopsy?
-a large area of tissue around the cervix is excised for examination
***Pathognomonic (spelling?) for Trichomoniasis?
-Strawberry cervix
*Menopause
-d/t hypo-estrogen, d/t ovarian failure, it is the cessation of period for 12 months
-avg age is 51
-hot flashes bc thermoreg center in the hypothalmus is sens to estrogen
-also develop sever fatigue and depression b/c hot flash may prevent REM sleep
***What are some of the most important changes of menopause?
-h/a and hot flashes
-hair becomes thinner, teeth loosen and gums recede
-breasts droop and flatten, nips become smaller and flatten
-risk of cardiovasc disease
-skin and mucous membranes become drier (esp vag)
-body and pubic hair becomes thicker and darker
-stress or urge incontinence
***What about bone after menopause?
-drop in estrogen leads to decrease in the stimulation of osteoblasts which in turn leads to osteopenia and osteoporosis (-2.5 on bone dextra)
-MC fracture is vertebral
***What is the best way to reduce the short/long term sequaelae of menopause?
-give ESTROGEN b/c all that shit I just listed will reverse (for the most part)
-also remember that this will decrease cholesterol and triglycerides
*Climacteric?
-the physio phase of life which marks the transition from repro to non-repro stage
***Perimenopause
-the period immediately prior to and the first year after actual menopause
-characterized by wide fluctuations in hormone levels and intervals between menstrual periods
*note: 80 y/o can be give estrogen cream for their vagina but pills will not work
***Neonatal hyperbilirubinemia
-Total serum bilirubin (TSB) > 5mg/dL
-60% of term newborns
-complications: deafness, CP/Kernicterus
-JACHO alert- boys, full - term, and breastfed babies are at high risk
-MC in term of 35-38 wks and dehydrated/not drinking enough
*How and where does bilirubin get to where it becomes conjugated?
-binds to albumin in the blood stream and gets to the liver where it becomes conjugated
-in the SI it is then converted to urobilinogen where it is excreted in the feces or urine
****What are the 3 benign classifications of Jaundice?
1. Physiologic - elevated UCB aka "lipid soluble", TSB peaks at 5-6 mg/dL on d 3-4 and declines by day 10
2. Breast milk: elevated UCB, basically a prolongation of physiologic, takes longer for UCB to come down to adult levels, may have 2nd peak
3. Breast feeding: Elevated UCB, benign or pathologic w/ ele in 1st wk and worsens d/t dehydration; tx increase milk supply or formula
***Case 1: 2 wk white M presents w/ yellow discoloration of eyes, face and neck for 3 days. Exclusively breast fed. Healthy. PMHx: uncomp preg/delivery at 40 wks. PE: + yellow pig of skin, more evident w/ light palp, + icteric sclera. Labs: TSB 7.0, CBC nl. Dx?
-Breast MILK jaundice
***What are the 3 causes of hyperbilirubinemia?
1. Increased Bilirubin load
2. Decreased Bilirubin Congugation (d/t genetics or hypothyroid)
3. Impaired bilirubin excretion (elevated UCB or CB > 2 or 20% TSB)
***Increased Bilirubin load:

What does Coombs + indicate?
-Rh incompatibility, ABO incompatibility, minor Ag
***Rh Incompatibility
-when mother lacks Rh factor on RBC surface and her baby is born w/ Rh factor on his/her RBCs
-2x as common in whites vs blacks
-DOES NOT occur w/ 1st child***
-Tx: Rh Ig (Rhogam) given at 28 weeks to Rh neg prego and w/in 72 h after birth if baby is Rh POS
*if already sens to Rh (has Abs) then injection is ineffective
***ABO incompatibility
-MC if mother type O and infant is A, B, or AB
-fetal cells cross placenta, mother forms Ab to fetal cells, cross back into baby and destroy RBC --> increased bilirubin -> hyperbilirubinemia
***ABO hemolytic disease of the newborn
-MC mother O and infant A or B
-***Significant EARLY jaundice (Coombs neg) <24 h
-****Spherocytes found on blood smear
-tx: phototherapy
***Increased Bilirubin load:

What does Coombs - indicate
***G6PD deficiency--> this enzyme initiates redox rxns in pentose pathway and is responsible for gluthatione and also reduces NADP to NADPH with overall effect of neutralizing free radicals
-deficiency of this enzyme leads to increase of free radicals which cause hemolysis of RBCs --> increase [bilirubin] --> kernicterus
***What is impaired bilirubin excretion d/t?
-common w/ biliary obstruction such as:
-structural (biliary atresia)
-genetic (Rotors/Dubin johnson
-Infection like sepsis and TORCH
***What is the gold standard for diagnosis?
-Test for hyperbilrubinemia w/ blood levels NOT just looking at the yellow child
-dermal zones should be used as a "mild screening test"
-best correlation is jaundice to the nipple line and bilirubin > 12 mg/dL
***Dermal Zones of jaundice:

What is the TSB (mg/dL) at each of following zones? (I doubt this is a TQ)
1. Face and neck: 4.5-5.8
2. Chest and back: 5.5 - 12
3. Abd below umb to knees: 8-13.6
4. Arms and legs below knees: 11-18
5. Hands and feet: >15
How many times a day should the child urinate?
-4-5 x otherwise sign of dehydration
***High risk baby for hyperbilirubinemia?
-Major risk factors are full term
-our note taker also writes, "preemie, aspyxia, and + fam hx -> would be a high risk baby"
***Tx for hyperbilirubinemia?
*Phototherapy - converts bilirubin into excretable water soluble form
-uses flourescent lighting or fiber optic blankets
-Goal: dec TSB by 4-5 mg/dL/day
-slower response in breast fed
-severe rebound hyperbilirubinemia CAN occur
-outcome is relative to total amount of area exposed
*Complications of hyperbilirubinemia?
-toxic to BG and brainstem nuclie
-acute bilirubin encephalopathy
-kernicterus
-Risk: TSB > 25-30 mg/dL, acidosis, female, increased free bili, drug displacement, prematurity, ischemia
*Risks for severe hyperbilirubinemia?
-jaundice in first 24 hours
-visible jaundice at discharge
-near term gestation 35-38 wks
-birth trauma (bruising, cephalohematoma, etc) --> more RBC lysis --> more bili
***What is an ectopic pregnancy?
-When an embryo implants anywhere outside of the uterine cavity
****What is a Cornual pregnancy?
-in the part of the fallopian tube that penetrates the uterine muscle, but NOT in the cavity
-are serious, terrible location for surgeons d/t huge blood supply and space for the ectopic to get very large (7-8 cm "orange sized") which can rupture leading to complete hysterectomy
***What is the MC site for an ectopic pregnancy?
- Isthmus of Fallopian tube
-woman will start feeling abd pain, and embryo is golf ball sized when it ruptures
***Women who are pregnant are _______ until proven otherwise?
1. Ectopic
2. Rh Neg
Case 1: 18 y/o G1P0 is prego at 7 weeks gestation, 2 d hx of vaginal spotting and severe lower abd pain. Vitals nL. Heart exam nL, abd is NON TENDER and no masses are palpated?
-ectopic prego
-this could be a miscarriage b/c vaginal spotting is miscarriage until proven otherwise
*Incomplete abortion vs complete abortion
1. Incomplete: fetus stuck to cervix
2. Complete: woman feels something fall into the toilet, this fetus and tissues "looks like a worm" (r/o eating at Arbys) then has spotting after all fetal tissue passed
***US and PE for the Case 1 pt
1. PE: uterus is of 4 weeks size (instead of 7 w based on menses) and non tender
-quant B-hCG is NOW 700 mlU/mL
2. TVUS reveals an empty uterus and no adnexal masses
*What is the discriminatory zone?
=1500 - 2000 mlU/mL B- hCG
-threshold where US can visualize an intra uterine sac
-B-hCG values above this zone w/out visualization of gestational sac signifies ectopic pregnancy
*What is the next step in management of this pt?
-in normal pregnancies the B-hCG doubles every 72 (NOT 7!!!!!!!)
-in ectopic pregos, the B-hCG increase is less than double
-for this pt it should be 1400, but it is currently 7000
*Serum progesterone
-if B-hCG is repeated several times and still low order this (it is not used often according to the hand out)
-5-20 ng/mL - ectopic (handout says less than 5)
-greater than 12 is normal
***What is a heterotopic pregnancy?
-one in uterus and one in tubes
-MCC = IVF b/c they put in 3-5 embryos per treatment cycle
-tx this w/ laparoscopic salpingectomy
***if the hCG is NOT zero then....
-think ectopic somewhere
-if looking at empty uterus but high hCG (3000) do bilateral salpingectomy
-***0% chance of prego in future
-if hemodynamically stable lowere hCG w/ DOC MTX injection
***Ectopic RFs
-PID
-Previous Hx ectopic pregnancy***
-15% recurrent risk
From handout:

*What represents a leading cause of maternal mortality and morbidity?
-Ectopic pregnancy
From handout:

*Arias-Stella Reaction
-neoplastic appearing endometrial glandular changes, usually focal
-while suggestive of ectopic preganancy may also be found in nL prego
From handout:

When the uterine mucosa is cast off for whatever reason, such a cast may be misdiagnosed as?
-an incomplete abortion unless histological evaluation is performed and demonstrates the ABSENCE of CHORIONIC VILLI
From handout:

What are the 3 classical clinical presentations of ectopic pregnancy"?
1. abd pain
2. amenorrhea
3. vaginal bleeding
(only 15% of pts present w/ all 3
From handout:

*How is ectopic pregnancy best R/O?
-using both TVUS and B-hCG testing
-a pt w/ no evidence of intrauterine gestation and a B-hCG value exceeding 2500 mIU/ml or a value that plateaus should be presumed to have an ectopic pregnancy until proven otherwise
From handout:

*Discriminatory Zone
-level of the B subunit of hCG above which a pregnancy (yolk sac) will be US visualized in utero
****serial quatitative B-hCG levels should double every 72 hours in normal pregnancy
From handout:

*With US how is dx of ectopic usually made?
-by ruling out an intra-uterine pregnancy when the level of the B-hCG is above the discriminatory zone
From handout:

*Salpingectomy is indicated for?
1. Ruptured ectopic and/or hemodynamically unstable
2. Patients wishing to avoid future pregnancy
***what if pt is hemodynamically stable and wants to potentially get prego in the future? give MTX