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131 Cards in this Set
- Front
- Back
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*Physiologic Tremor
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-predominantly in the hands
-increased w/ epi and adrenergic stimulants -DEC w/ ETOH and B-adrenergic blocking agents |
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Cerebellar Tremor
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-intention, ataxic, rubral
-occurs at the end of a purposeful movement |
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***Parkinson's Tremor
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-resting tremor that disappears w/ action
-frequency 3-5 hz -"pill rolling" -increased w/ stress -decreased w/ Dopaminergic agents |
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***Essential (Familial, Senile)
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-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) |
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***Head tremor is seen in ________ but NOT _____?
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-Essential tremors but NOT Parkinson's disease
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What are treatments for Essential Tremor?
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-Propranolol - most effective B-blocker: decreases amplitude of tremor
-primidone -gabapentin, benzodiazepenes, pregabalin may also help -DBS of thalmus |
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***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????) |
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***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) |
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*Chorea
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-abnormal involuntary movement disorder
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Athetosis
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-continuous stream of slow, sinuous, writhing movements
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Ballismus
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-violent involuntary rapid and irregular movements
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Dystonia
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-sustained muscle contractions which cause twisting and repetitive movements or abnormal postures
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***Asterixis
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-tremor of the wrist when the wrist is extended (flapping tremor)
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***Primary Torsion Dystonia (aka Dystonia musculorum deformans)
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-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 |
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***Wilson's Disease
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-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) |
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What are the labs for Wilson's
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-Dec ceruloplasmin
-increased serum copper -increased urinary copper -liver biopsy shows copper deposition (usually liver presents earlier) |
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What are some of the neuro-pyschiatric sx?
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-mild cog impairment, clumsiness, ataxia, tremor, parkinsonism, depression...etc
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***What is the tx of Wilson's
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-chelation using agents which bind Cu and remove Cu deposits (penicillamine)
-Trientene hydrochloride is the DOC |
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***Huntington's disease
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-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 |
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***HD is a true _____
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-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 |
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*Juvenile HD
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-under 20
-progressive parkinsonism, ataxia, dementia, and seizures -80 repeats of CAG likely juvenile HD -L-Dopa for parkinsonism in Juvenile HD |
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Tx of HD
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-benzodiazpines for anxiety
-antidepressants and antipyschotics |
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***CT/MRI will show?
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-loss of volume of caudate nucleus and putamen
-PET will show decreased flouro deoxy glucose metab in striatum |
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***Acute dystonic rxns may occur w/?
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-Antiemetics - REGLAN
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***Akathisia
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-inability to remain in a sitting position
-motor restlessness and feeling of muscular quivering (not seen) |
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***Tardive Dyskinesia
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-bucal, lingual, masticatory dyskinetic movements common
-MC appears w/in 3 months of withdrawal from DOPAMINE BLOCKERS (neuroleptics, reglan) |
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***What are the 4 cardinal signs of parkinsonism?
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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) |
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*Rigidity of PD
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-increase in muscle tone best tested at wrist, elbow, or neck
-cogwheel/rachet - like character when muscle tone is tested |
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*Akinesia
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-masked faces
-difficulty initiating movement -decreased blinking and swallowing -decreased force of speech (hypophonia) -difficulty rising from chairs or turning in bed |
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*Posture in PD
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-retropulsive: tendency to fall back
-forward stoop -unsteady-uncertain - in turning or on stairs |
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Early PD
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-bradykinesia (hallmark)
-resting tremor in 80% -asymmetry -tremor dominant cases have good prognosis -rigid-akinetic cases progress more rapidly -NO postural or impaired balance |
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Later stage PD
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-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 |
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*Atypical parkinsonism
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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) |
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***Non motor sx of PD
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-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) |
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NYCOM study for PD
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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 |
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What did the OMT tx for the PD pts consist of?
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-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
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***Conclusions of the study
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-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 |
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**OPP and MS
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-direct MFR and ME addresses spasticity
-cranial techniques: addresses balance and coordination |
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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?
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-MIXED (b/c she leaks w/ valsalva (sneeze/cough) and has a strong urge to void w/ dysuria
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***Genuine Stress Incontinence
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-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 |
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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 |
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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 |
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From handout:
*Any time the sum of the intra-abd pressure + ________ exceeds the _____ urine will come out |
-bladder pressure exceeds the urethral closing pressure
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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 |
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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 |
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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 |
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***Urge incontinence
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-"detrusor instability"
-loss of urine d/t an uninhibited and sudden bladder contraction (overcomes ones conscious input to hold urine) |
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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 |
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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
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***Overflow incontinence
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-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) |
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***How do you tx overflow incontinence?
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-Tx w/ behavioral modification (pee schedule) bc neither surgery or medication will help
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From handout:
Total incontinence |
-abnormal drainage situations (ie fistulae, diverticulae, ectopic ureter)
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****Reversible forms of incontinence:
DIAPPERS |
-Delirium
-Infection -Atrophic vagininitis -Psychological -Pharmacologic -Excess fluid -Restricted mobility -Stool impaction |
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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 |
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*Atrophic Vaginitis
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-at menopause d/t lack of estrogen
-bladder is estrogen dependent (has lots of collagen) -Tx: estrogen |
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*Pyschological
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-when leak urine and stool when depressed
-tx SSRI, antidepressants |
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*Excess Fluid states
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-DM, SIADH, periph edema, CHF
-tx: furosemide (diuretic) |
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*Restricted mobility
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-ex in nursing homes
-tx: pt should be assisted to bedside commode every hour one the hour while awake |
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*Stool impaction
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-decreases relative capacity of the bladder
-tx: disimpaction, enema |
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*Risks for incontinence
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-obesity
-prego (especially w/ big babies b/c stretches the vesicoureteral junction) |
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From handout:
** a dx of GUSI is suggested by... |
continence while lying down and spurts of urine SIMULTANEOUS w/ increases in intra abd pressure
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From handout:
** a dx of DI is suggested by... |
urgency, frequency, nocturia, enuresis and supine incontinence
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From handout:
** a dx of OVERFLOW is suggested by... |
-loss of small amounts of urine + frequent voiding of small amounts
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From handout:
** a dx of ATROPHY is suggested by... |
=hypoestrogenic states (ie menopause, lactation, oophorectomy)
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***Why is limping in a child such a complicated issue?
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-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) |
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*DDx of Limp for ALL ages
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-septic arthritis
-osteomyelitis -stress fracture -neoplasm -marrow swelling (leukemia) -neuromuscular (musc dystrophy) |
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***DDx of Limp for TODDLER
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-developmental hip dysplasia
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***DDx of Limp for 3-10 y/o
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1. Legg-Calve-Perthes
2. Juvenile RA 3. Toxic synovitis |
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*DDx of Limp for adolescents
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-slipped capital femoral epiphysis (essentially a femoral head fracture)
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***Septic arthritis
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-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 |
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***Toxic (Transient) synovitis
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-***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 |
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***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 |
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*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?
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-drain in OR
-Abx for weeks (if bone involvement requires 6 weeks of abx) |
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***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?
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-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 |
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**Legg-Calve-Perthes
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-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) |
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*Case 3: 3 y/o M w/ limp this morning/ had an URI 1 week ago that resolved. Left hip pain. Labs normal. Dx?
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-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) |
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*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?
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-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 |
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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...
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-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) |
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***Aproximately how many women suffer from cervical cancer in the USA and then in the rest of the world?
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-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 |
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*List or describe as many of the causes of cervical CA that you can?
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-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 |
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*List as dx tools that the average "run of the mill physician" might utilize to workup and dx of cervical cancer?
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-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 |
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***Findings that may be found in cervical CA?
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-increase mitotic features, blood, koilocytosis, finger like projections, hyperchromatin, loss of cell polarity
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* List some of ways cervical CA may be tx in pts w/ diagnosis. Surgical and medical?
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-Leap and cone
-Radical hysterectomy -Wide excision -chemo |
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* If surgery did not go well and pt looks like they are going into shock...
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-fresh frozen plasma
-nL saline -intubate *this is a fucking stupid question |
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*What is a cold cone biopsy?
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-a large area of tissue around the cervix is excised for examination
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***Pathognomonic (spelling?) for Trichomoniasis?
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-Strawberry cervix
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*Menopause
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-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 |
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***What are some of the most important changes of menopause?
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-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 |
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***What about bone after menopause?
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-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 |
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***What is the best way to reduce the short/long term sequaelae of menopause?
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-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 |
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*Climacteric?
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-the physio phase of life which marks the transition from repro to non-repro stage
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***Perimenopause
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-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 |
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***Neonatal hyperbilirubinemia
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-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 |
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*How and where does bilirubin get to where it becomes conjugated?
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-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 |
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****What are the 3 benign classifications of Jaundice?
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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 |
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***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?
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-Breast MILK jaundice
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***What are the 3 causes of hyperbilirubinemia?
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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) |
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***Increased Bilirubin load:
What does Coombs + indicate? |
-Rh incompatibility, ABO incompatibility, minor Ag
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***Rh Incompatibility
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-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 |
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***ABO incompatibility
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-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 |
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***ABO hemolytic disease of the newborn
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-MC mother O and infant A or B
-***Significant EARLY jaundice (Coombs neg) <24 h -****Spherocytes found on blood smear -tx: phototherapy |
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***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 |
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***What is impaired bilirubin excretion d/t?
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-common w/ biliary obstruction such as:
-structural (biliary atresia) -genetic (Rotors/Dubin johnson -Infection like sepsis and TORCH |
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***What is the gold standard for diagnosis?
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-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 |
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***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 |
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How many times a day should the child urinate?
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-4-5 x otherwise sign of dehydration
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***High risk baby for hyperbilirubinemia?
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-Major risk factors are full term
-our note taker also writes, "preemie, aspyxia, and + fam hx -> would be a high risk baby" |
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***Tx for hyperbilirubinemia?
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*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 |
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*Complications of hyperbilirubinemia?
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-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 |
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*Risks for severe hyperbilirubinemia?
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-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 |
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***What is an ectopic pregnancy?
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-When an embryo implants anywhere outside of the uterine cavity
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****What is a Cornual pregnancy?
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-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 |
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***What is the MC site for an ectopic pregnancy?
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- Isthmus of Fallopian tube
-woman will start feeling abd pain, and embryo is golf ball sized when it ruptures |
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***Women who are pregnant are _______ until proven otherwise?
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1. Ectopic
2. Rh Neg |
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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?
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-ectopic prego
-this could be a miscarriage b/c vaginal spotting is miscarriage until proven otherwise |
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*Incomplete abortion vs complete abortion
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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 |
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***US and PE for the Case 1 pt
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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 |
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*What is the discriminatory zone?
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=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 |
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*What is the next step in management of this pt?
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-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 |
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*Serum progesterone
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-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 |
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***What is a heterotopic pregnancy?
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-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 |
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***if the hCG is NOT zero then....
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-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 |
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***Ectopic RFs
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-PID
-Previous Hx ectopic pregnancy*** -15% recurrent risk |
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From handout:
*What represents a leading cause of maternal mortality and morbidity? |
-Ectopic pregnancy
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From handout:
*Arias-Stella Reaction |
-neoplastic appearing endometrial glandular changes, usually focal
-while suggestive of ectopic preganancy may also be found in nL prego |
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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
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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 |
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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 |
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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 |
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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
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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 |
