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PAGET'S DISEASE PATHOPHYSIOLOGY: EXCESSIVE BONE TURNOVER BY OSTEOCLASTS +/- ASSOCIATED WITH PARAMYXOVIRUS INFECTION
PAGET'S S/S: DEEP BONE PAIN
FREQUENT #
INCREASED CRANIAL DIAMETER (=FRONTAL BOSSING)
DEAFNESS D/T CN VIII COMPRESSION
PAGET'S LAB & XRAY FINDINGS: INCREASED ALP, URNIARY HYDROXPROLINE
NORMAL Ca, PO4
XRAY - MARKEDLY EXPANDED BONY CORTEX - INCREASED DENSITY, THICKENED TRABECULAE, CHARACTERISTIC "JIGSAW" OR "MOSAIC" BONE PATTERN
PAGET'S - Rx: NSAIDS, CALCITONIN, ALENDRONATE
Paget's - complications: #'s, high output cardiac failure, deafness, secondary osteosarcoma
heliotrope rash: violacious periorbital rash in dermatomyositis
Grotton's papules: papules on dorsum of hand over bony prominences in dermatomyositis
polymyositis lab and EMG findings: elevated serum creatine, aldolase, CPK
EMG - fibrillations
complications of polymyositis: myocarditis, cardiac conduction defects, malignancy
Felty's triad: hepatosplenomeagly
TCP
RA
Lab, synovial fluid and Xray findings in RA: rh factor = anti-Fc IgG Ab - elevated in >75% (not specific)
+/- ESR elevated
synovial fluid - turbbid, decreased viscosity, WBC 3000-50000 cells/microL
Xray - juxta-articular dimineralization (early) joint space narrowing and erosions (late)
JRA - most common type?: pauciarticular - <30% develop iridocyclitis
ANA type - most common - asymmetric involvement of large joints with iridocyclitis
RF type - poor Px - concurrent with AS in HLA-B27+ males
Systemic acute febrile JRA: least common
characteristic arthritis with daily high spiking fevers
evanescent salmon coloured rash
+/- hepatosplenomegaly and serositis
Scleroderma S/S: thickening of skin of face +/or distal extremities
CREST
severe form - pulmonary fibrosis, cor pulmonales, ARF, malignant HTN
Anticentromere Ab: specific for CREST
anti-Scl-70 = anti-topoisomerase 1: specific for systemic scleroderma
treatment for scleroderma: glucocorticoids, penicillamine for skin changes, CCB for Raynaud's, ACEI for renal dz/HTN
SLE criteria: DOPAMINE RASH =
Discoid rash
Oral ulcers
Photosensitivity
Arthritis
Malar rash
Immunologic criteria
Neurologic symptoms (lupus cerebritis, seizures)
Elevated ESR
Renal disease
ANA +
Serositis
Hematologic abnormalities - anemia, leukopenia, TCP
Anti-dsDNA, Anti-Sm Ab's: highly specific, not sensitive for SLE
drug induced SLE antibodies: Antihistone Ab
Anti-Ro Ab's: neonatal SLE
Anti-phospholipid Ab's: hypercoagulability, thromboembolic disease, recurrent spontaneous abortions
Rx for SLE: NSAIDs (initial)
Steroids for acute exacerbations
hydroxychloroquine, cyclophosphamide, azithroprine for progressive/refractory cases
SLE pathogenesis, epidemiology: 90% female (esp. African American)
Antibody-mediated cellular attack with deposits of antigen-antibody complexes
Drugs inducing SLE: hydralazine
pencillamine
procainamide
Temporal arteritis pathogenesis: subacute granulomatous inflammation of large vessels (includes aorta, ext. carotid - temp. br, vertebral a's)
temporal arteritis S/S: new h/a uni/bilateral with scalp pain
temporal tenderness
jaw claudication
fever
transient/perm monocular blindness
+/- wt loss, myalgia/arthralgia
bx findings in temporal arteritis: thrombosis, media necrosis, lymphocyes, plasma cells, giant cells
HSP path and epi: immune mediated small vessel vasculitis
children 2-11 y/o
HSP S/S: palpable purpura on buttocks, legs
asym. migartory periarticular swelling
abdominal pain
preceding URTI (75%)
Complications of HSP: GIB, intussusception, GN - degree of renal involvment determines Px
Barlow's maneuver: for DDH
pressure on inner aspect of abd thigh, hip add - causes post. dislocation
Ortolan's maneuver: for DDH
thighs abdocuted from midline with anterior pressure on greater trochanter - +ve = soft click (femoral head reduced into acetabulum)
Allis'/Galeazzi's sign: for DDH
knees at unequal heights when baby's hips and knees flexed (dislocated side lower)
Evaluation of DDH: clinical, U/S esp after 10 weeks old (not xray until >4m old)
Monteggia's #: diaphyseal # of prox ulna with subluxation of radial head
Galeazzi's #: diaphyseal # of radius with dislocation of distal r/u joint - d/t direct blow to radius
Rx - ORIF radius, cast in supination to reduce r/u jt
clavicular #: most common #'d long bone in kids
can be associated with brachial plexus injuries
greenstick #: incomplete # - cortex of only one side of bone
Rx - reduction with casting, repeat Xray 7-10days
nursemaid's elbow: radial head subluxation secondary to child being pulled or lifted by the the hand
Rx - gentle supination of elb at 90
Torus #: buckling of cortex of long bone secondary to trauma
- usually distal radius or ulna
Salter-Harris # type I: physis
Salter-Harris # type II: metaphysis and physis
Salter-Harris # type III: epiphysis and physis
Salter-Harris # type IV: epiphysis, metaphysis, physis
Salter-Harris # type V: crush injury of physis
Rx of Salter-harris #'s: Types I, II - conservative
III - V - Sx
Rx of DDH: Splint with Pavlik harness (maintains hip flexed, abd) if <6m old
6-15m old - spica cast
15-24m old - ORIF
DDx of limp in children: "STARTSS HOTT"
Septic joint
Tumor
AVN (LCPD)
RA/JRA
TB
SCA
SCFE
HSP
Osteomyelitis
Trauma
Toxic synovitis
osteosarcoma: 2nd most common primary malignancy of bone (MM 1st)
metaphyseal region of distal femur, prox. tibia, prox. humerus - mets to lungs
males, 2nd-3rd decades
osteosarcoma vs Ewing's: Osteo
metaphyseal region distal femur, prox tibia/humerus
Xray - Codman's triangle, "sunburst" pattern
Ewing's
diaphyseal-metaphyseal regions of pelvis, femur, tibia
multilayered "onion-skinning"
Codman's triangle: Osteosarcoma Xray finding = periosteal new bone formation at diaphyseal end of bone
lesion of Broca's area: Broca's aphasia - motor (expressive) - broken speech, normal comprehension
lesion of Wernike's area: sensory (fluent/receptive)aphasia - poor comprehension
lesion to arcuate fasciculus: conduction aphasia - poor repitition with good comprehension, fluid speech
Lesion to amygdala bilaterally: Kluver-Bucy syndrome - hyperorality, hypersexuality, disinhibited behaviours
lesion to fronal lobe: frontal release signs - personality changes
deficits in concentration, orientation, judgement
right parietal lobe lesion: spatial neglect syndrome - agnosia of contralateral side of the world
Lesion to mamillary bodies bilaterally: Wernicke-Korsakoff's encephalopathy - confabulations, anterograde amnesia
CN XII lesion: tongue deviates towards lesion side
CN V lesion: jaw deviates towards
unilateral cerebellum lesion: patient falls towards side of lesion
CN X lesion: uvula deviates AWAY from lesion side
CN XI lesion: head turns towards side of lesion
R optic nerve defect: right hemianopsia
optic chiasm lesion: bitemporal hemianopsia
R optic tract lesion: L homonymous hemianopsia
R Meyer's loop lesion: L upper quadrant anopsia = right temporal lesion
R dorsal optic radiation lesion: L lower quadrant anopsia = R parietal lesion
R visual cortex lesion: L hemianopsia with macular sparing
anterior cerebral artery distribution: medial surface of brain, leg-foot area of motor and sensory cortices
middle cerebral artery distribution: lateral aspect of brain, Broca's and Wernicke's areas
Anterior communicating artery defects: most common circle of Willis aneurysm, +/- visual field defects
Posterior communicating artery defects: CN III palsy
common area of aneurysm
Lateral striae arteries distribution: internal capsule, caudate, putamen, globus pallidus = "arteries of stroke"
stroke of anterior Circle of Willis: general sensory and motor dysfunction, aphasia
Stroke of posterior Circle of Willis: vertigo, ataxia, visual defects, coma
Poliomyelitis/Werdnig-Hoffman disease spinal cord lesions: LMN lesions only = flaccid paralysis
MS spinal cord lesions: mostly white matter of cervical region - random and asym lesions
ALS: combined U/LMN deficits
NO sensory deficits
Anterior spinal artery lesion: spares dorsal columns
Tabes dorsalis: impaired propriocetion
locomotor ataxia
d/t tertiary syphilis
syringomyelia: affects ventral white commissure and ant. horns
Vit B12 neuropathy/Friedreich's ataxia: affects dorsal columns, lateral corticospinal and spinocerebellar tracts
Broca's aphasia: disorder of language production with intact comprehension - pts aware
impaired repitition
Associated with arm and face hemiparesis (right), hemisensory loss, apraxia of oral muscles
d/t L superior MCA stroke
Wernicke's aphasia: disorder of language comprehension
neologisms, paraphasic errors
pts unaware
no hemiparesis, dysarthria
L inf/post MCA embolic stoke
poor Px c/w Broca's
Locked in syndrome S/S, causes: awake and alert, unable to move except eyes and eyelids
central pontine myelinolysis
brain stem CVA
advanced ALS
Persistent vegetative state: normal sleep-wake cycles
most common - diffuse cortical injury
hypoxic-ischemic injury
5 A's of dementia: Aphasia
Amnesia
Agnosia
Apraxia
disturbances in Abstract thought
Causes of dementia: "DEMENTIAS"
neuroDegenerative diseases
Endocrine
Metabolic
Exogenous
Neoplasm
Trauma
Infection
Affective disorders
Stroke/Structural
Peripheral vs central vertigo: Peripheral - intermittent, severe, constant nystagmus, always horizonal, unidirectional, associated with hearing loss, no brain stem S/S
Central - constant, less severe, +/- nystagmus (absent, uni/bidirectional, +/- vertical)Rare hearing loss, often brain stem S/S (ataxia, dysarthria, CN abN, motor dysfunctions)
Most common causes dysequilibrium: BPPV (50%)
Ménière's
Others - hypothyroid, aminoglycoside/furosemide toxicity, stroke, trauma, labyrinthitis, acoustic neuroma
Nylen-Barany Maneuver: = Dix-Hallpike maneuver
pt sitting to supine quickly turning head to side - +ve if reproduces vertigo +/or nystagmus = BPPV
BPPV S/S: transient episodic vertigo <1min
nystagmus triggered by changes in head position (classic - turning in bed/getting up in am)
N/V
Symptoms decrease with repetitive testing
Meniere's disease S/S (=endolymphatic hydrops): intermittent peripheral vertigo d/t distention of endolymphatic compartment of inner ear
N/V
ear fullness
hearing loss
tinnitus
episodes resolve hrs-days
Causes of Meniere's: head trauma
syphilis
audiometry findings in Meniere's: low-frequency pure-tone hearing loss
Treatment of Meniere's: low salt diet
acetazolamide
actue attacks - antihistamines, antiemetics, benzo's
surgical decompression if refractory
acute h/a causes: SAH
hemorrhagic CVA
meningitis
seizure
acutely increased ICP
hypertensive encephalopathy
post-LP
ocular dz (glaucoma, iritis)
new migraine
subacute h/a causes: temporal arteritis
intracranial tumor
SDH
pseudotumor cerebri
trigeminal/glossopharyngeal neuralgia
post-herptic neuralgia
HTN
chronic/episodic h/a causes: migraine
cluster h/a
tension h/a
sinusitis
dental dz
neck pain
Migraine h/a S/S: throbbing h/a >2hrs, <24hrs
N/V
photophobia
noise sensitivity
"Classic" - u/l, visual aura (scintillating scotomas or field cuts)
"common" - b/l, periorbital without associated symp
Treatment of migraine h/a: ASA/NSAIDS, triptans
prophylaxis - BB, TCA, CCB, valproic acid
Cluster h/a description: brief, severe, usually u/l periorbital h/a 30min-3hrs
affects same part of head, same time of day (night), same time of year
triggers - EtOH, vasodilators
Cluster h/a S/S: ipsilateral tearing of eye
conjunctival injection
Horner's syndrome
nasal stuffiness
Treatment of cluster h/a: acutely - high flow O2 (100% non-rebreather)
ergots
sumatriptan
intranasal lidocaine
corticosteroids
Prophylaxis of cluster h/a: ergots
CCB
prednisone
lithium
valproic acid
topiramate
SAH causes: ruptured aneurysm (berry)
AVM
trauma (most common)
Berry aneurysms associated with?: PcKD
coarctation of aorta
CN involvment in SAH: CN III palsy with pupil involvement associated with Berry aneurysms
Treatment of SAH: prevent rebleeding - most likely in 1st 48hrs
prevent vasospasm - nimodipine and IV fluids, maintain elevated BP
antiseizure meds - phenytoin
NO NSAIDs
Complications of SAH: rebleeding aneurysm>AVM
extension into brain parenchyma (AVM)
vasospasm (in 1/3 of aneurysmal SAH)
obstructive hydrocephalus
EDH CT findings: lens-shaped CONVEX hyperdensity
SDH CT findings: cresent-shaped, CONCAVE hyperdensity
parenchymal hemorrhage causes: HTN - usually in basal ganglia
tumor
amyloid angiopathy (elderly)
vascular malformations (AVM, cavernous hemangiomas)
Cushing's triad: alterations in BP, HR, and respiratory patterns
Parkinson's tetrad: resting tremor
bradykinesia
rigidity
postural instability
treatment of parkinson's: dopamine agoinsts - brompcriptine, levo/carbadopa
MAO-B inhibitors - selegiline (neuroprotective, decreases levodopa need)
COMT inhibitors - entacapone (increase levodopa availability, may decrease motor fluctuations)
(amandatine, antiAch - limited efficacy)
astrocytomas: Adults
S/S h/a, increased ICP
+/- u/l paralysis CN V-VII, X
slow, protracted course
Rx - resection, XRT
GBM: most common primary
h/a, increased ICP
rapid progression, poor Px (<1yr)
meningiomas: women>men
from dura or arachnoid
increased incidence with age
acoustic neuroma: ipsilateral hearing loss
tinnitus
vertigo
signs of cerebellar dysfunction
Derived from Schwann cells
Medulloblastoma: children
from 4th vent - increased ICP
highly malignant - can seed subarachnoid space
Rx - Sx + chemo + XRT
ependymoma: children
from ependyma of ventricle (4th) or spinal cord
hydrocephalus
Rx - Sx + XRT
Neurocutaneous syndromes: NF 1,2
Tuberous sclerosis
NF 1 mutation: NFT-1 gene on 17q
NF 2 mutation: defective gene chrom. 22
NF1 diagnostic criteria: >=2 of:
1) 6 cafe au lait spots (>5mm kids, 15mm adults)
2) 2 neurofibromas (any type)
3)feckling-axillary/inguinal
4) optic glioma
5) 2 Lisch nodules = pigmented iris hamartomas
6)osseus abnormalities
7) 1st degree relative
NF2 diagnostic criteria: bilateral acoustic neuromas
1st degree relative
unilateral acoustic neuroma
any 2 of:
neurobfibroma
meningioma
glioma
schwannoma
Other features (not criteria)
seizures, skin nodules, cafe-au-lait spots
Tuberous Sclerosis - characterized by:: seizures (begin <1y/o)
mental retardation
skin and eye lesions
Tuberous sclerosis - presentation: infantile spasms
ash-leaf hypopigmented lesions
(trunk and extremities)
Skin lesions in tuberous sclerosis: sebaceous adenomas (small red nodules over nose and cheeks like acne)
shagreen patch (rough papule in L/S region with orange peel consistency)
Ash-leaf hypopigmented lesions (trunk and extremities)
Retinal lesions in tuberous sclerosis: mulberry tumors (arise from nerve head)
phakomas (round, flat, grey lesions near disc)
Tests and findings in Tuberous sclerosis: calcified tubers in periventricular area (rarely transform into malignant asyrocytomas)
Skin lesions with Wood's lamp
ECG for rhabdomyoma (apex of LV in 50% pts)
Renal U/S - renal hamartomas, PcKD
Pulmonary - angiomyolipomas (cause generalized cystic or fibrous changes)
Thiamine deficiency: Wernicke's encephalopathy
Korsakoff's dementia
Wernicke's encephalopathy: triad = encephalopathy, ophthalmoplegia (LR palsy,nystagmus, conjugate gaze palsy), ataxia (polyneuropathy, CB and ventricular dysfunction)
Korsakoff's dementia: Wernicke's (encephalopathy, ophthalmoplegia, ataxia) + amnesia, horizontal nystagmus
Way to elicit Wernicke's encephalopathy: Large dose glucose administration
Cyanocobalamin deficiency: = B12 deficiency
Combined system disease or subacute combined degeneration
Cyanocobalamin deficiency S/S: gradual, progressive onset
symm. P/N
leg stiffness
spasticity
paraplegia
bowel/bladder dysfunction
Dementia
Folate deficiency: irritability
memory loss
personality changes without CSD of B12
Seizure causes in infants: perinatal injury
infection
metabolic
congential
Childhood (2-10y/o) causes of seizures: idiopathic
infection
trauma
fever
Adolescent causes of seizures: idiopathic
trauma
drug withdrawl
AVM
Young adult (18-35y/o) causes of seizures: trauma
alcoholism
brain tumor
Adult (>35y/o) causes of seizures: trauma
stroke
metabolic disorder
alcoholism
brain tumor
Lab finding in epileptic seizure: elevated prolactin
Simple partial seizures: motor, sensory, autonomic, or psychic features without LOC
+/- post-ictal focal neuro
deficit resolves 1-2 days
Can evole into generalized
DDx from acute CVA with MRI
Complex partial seizures: temporal lobe (70-80%)
char by:
impaired LOC
auditory/visual hallucinations
deja vu
automatisms
post-ictal confusion/disorientation, amnesia
Symp can mimic schizophrenia/acute psychosis
Can evolve into generalized
Normal EEG in seizure: Does NOT r/o epileptic sz disorder
First line anti-convulsant in children: phenobarbital
1st line treatment of idiopathic generalized seizures: Valproic acid
Adjuncts - lamotrigine, topiramate
treatment of secondary tonic-clonic seizures: Same as partial seizures
Absence seizures EEG finding: 3/sec spike-and-wave discharges (classic)
Absence seizures treatment: ethosuximide - 1st line
Valproic acid, zonisamide
West syndrome: Infantile spasms
Abnormal interictal EEG (v. high amplitude slow waves)
Arrest of psychomotor devt at age of sz onset
West syndrome S/S: begins 3-12m
sz - tonic, b/l, symm in clusters of 5-10 individual spasms - occur when drowsy or on awakening
MR in most pts
West syndrome Rx: ACTH
prednisone
anti-epileptics (clonazepam, valproic acid)
Status epilepticus definition: prolonged (>30min) or repetitive sz without a return to baseline
20% mortality
Status epilepticus causes: anticonvulsant withdrawl/non-comliance
anoxic brain injury
EtOH/sedative withdrawl
drug intoxication
metabolic - hyponatremia
trauma
infections
Treatment of Status epilepticus: ABC's
IV benzo + phenytoin loading dose
If sz continue - intubate + phenobarbital loading dose
glucose, thiamine, naloxone
Risk factors for CVA: non-modifiable - male, age, genetics, race (African-American, Hispanic, Asian)
Modifiable - HTN, DM, obesity, smoking, hypercholesterolemia, carotid stenosis, heavy EtOH, cocaine, IVDU, AFib
CVA most common etiology: athlerosclerosis of extracranial vessels (internal and common carotids, basilar, vertebral)
Underlying causes of lacunar infarcts: athlerosclerosis
HTN
DM
cardiac causes of CVA: Afib (risk increased 5-6x)
emboli - mural thrombi, diseased/prosthetic valves, paradoxic (venous) in R-to-L shunt (ASD, PFO)
MCA stroke S/S: aphasia (dominant hemisphere)
neglect (non-dominant)
contralat. hemiparesis, gaze preference, homonymous hemianopsia
ACA stroke S/S: leg paresis
amnesia
personality changes
foot drop
gait changes
cognitive changes
PCA stroke S/S: homonymous hemianopsia
memory deficits
dyslexia/alexia
Basilar stroke S/S: coma
CN palsies
apnea
visual symp
drop attacks
dysphagia
lacunar stroke S/S: pure motor or sensory
dysrthria-clumsy hand syndrome
ataxic hemiparesis
tPA contraindications: SBP >185 or DBP >110 despite aggressive antihypertensive Rx
prior ICH
CVA/head trauma in past 3m
recent MI
current anticoagulant Rx with INR >1.7
heparin in last 48hrs with increased PTT
platlets <100000
major Sx in last 14d
GI/GU bleed in past 21d
sz present at CVA onset
glucose <50/>400mg/dL
age <18
5 A's of Guillain-Barre: Acute inflammatory demyelinating polyradiculopathy
Ascending paralysis
Autonomic neuropathies
Arrhythmias
Albuminocytologic dissociation
Findings in Guillain-Barre: EMG/nerve conduction studies - diffuse demyelination
CSF - protein >55mg/dL with little/no pleocytosis
Myasthenia gravis antibodies: postsynaptic ACh receptor Ab (85-90%)
antistriational Ab (85% of pts with thymoma)
Labert-Eaton Syndrome antibodies: autoantibodies to presynaptic Ca channels
Myasthenia Gravis assoicated disorders: thymoma
thyrotoxicosis
autoimmune - SLE, RA
Myasthenia Gravis S/S: fatiguable ptosis/diplopia
dysphagia
proximal muscle weakness
symp worsen throughout day
"Myasthenic crisis": respiratory compromise and aspiration (rare)
Drug induced myasthenic syndrome cause: aminoglycosides
Myasthenia Gravis findings: edrophonium - dramatic improvement (diagnostic)
Abnormal single fiber EMG +/or decremental response to repetitive nerve stim
ACh Ab (85-90%)
Antistriational Ab (85% of pts with thymoma)
Treatment of MG: anticholinesterases - neostigmine, pyridostigmine
immunosuppressants - prednisone
Resection of thymoma - can be curative
ALS pathogenesis: loss of motor neurons in spinal cord, brain stem, and motor cortex
ALS S/S: asymmetric, slowly progressive weakness of arms, legs, CNs
UMN and LMN signs
Diagnostic findings in ALSq: Combination of U and LMN signs in >= 3 extremities
Findings in ALS: EMG/NCS - widespread denervation and fibrillation potentials
treatment in ALS: supportive
aggressive pulmonary toilet
Riluzole - reduces presynaptic glutamate release, may slow progression
Risk factors for carpal tunnel syndrome: repetitive use injury
pregnancy
DM
hypothyroid
acromegaly
RA
obesity
MS possible pathogenesis: T cell mediated autoimmune progression
MS classic triad: scanning speech
intranuclear ophthalmoplegia
nystagmus
Most common presenting complaints in MS: limb weakness
optic neuritis
P/N
diplopia
urinary retention
vertigo
Exacerbating factors in MS: infection
heat
trauma
vigorous activity
(decreasing - pregnancy)
MRI findings in MS: multiple, asymmetric, often periventricular white matter lesions
Corpus callosum lesions ~pathognomonic
Active lesions enhance with gadolinium
CSF findings in MS: mononuclear pleocytosis (>5cells/microL) 25%
elevated IgG - 80%
oligoclonal bands (non-specific) albuminocytologic dissociation
Treatment for MS: Steroids - acute exacerbations
Immunomodulators - ABC
Avonex/Rebif (interferon-β-1a)
Betaseron (interferon-β-1b)
Copaxone (copolymer-1)
Symtomatic Rx for spasticity, pain, fatigue, depression
Closed angle glaucoma epidemiology: elderly
Asians
Causes of closed angle glaucoma: acute closure of narrow anterior chamber angle ==>
pupillary dilatation - prolonged time in dark, stress, meds
ant. uveitis
dislocation of lens
Closed angle glaucoma S/S: extreme pain and blurred vision, ~always u/l
eye hard and red
pupil dilated, non-reactive to light
N/V
increased IOP
Treatment of Closed angle glaucoma: lower intraocular pressure - acetazolamide
pilocarpine once pressure drops
laser iridotomy - curative
open angle glaucoma risk factors: >40 y/o
FHx
African-American
DM
myopia
Open angle glaucoma pathogenesis: intraocular pressure increase d/t diseased trabecular meshwork that obstructs proper drainage of eye ==> gradual pressure increase causing progressive visual loss
Open angle glaucoma S/S: frequent lens changes in pts >35y/o
mild h/a
visual disturbances
impaired adaption to darkness
visual loss begins peripherally
Fundoscopic findings in open angle glaucoma: cupping of optic disc
Treatment of open angle glaucoma: preventative - >40y/o see ophthalmologist q3-5yrs (annual if increased RFs)
topical α-blockers - timolol, betaxolol (decrease aqu. humor producation)
pilocarpine (increases aqu. outflow)
carbonic anhydrase inhibitors if eye drops insufficient control of IOP
laser trabeculoplasty
Macular degeneration risk factors: Caucasian
female
smokers
FHx
Macular degeneration types: atrophic - gradual visual loss
exudative - more rapid and severe visual loss
macular degeneration S/S: painless loss of central vision
macular degeneration fundoscopy findings: pigmentary or hemorrhagic disturbances of macular region
treatment of macular degeneration: limited
laser photocoagulation may delay loss of central vision in exudative type
CRAO S/S: sudden, painlesss, u/l blindness
pupil accomodates
sluggish pupil reaction to direct light
CRAO fundoscopy findings: cherry-red spot on fovea
arteries +/- bloodless appearance
+/- retinal swelling
CRVO S/S: rapid painless vision loss
elderly pts
fundoscopy findings of CRVO: retinal hemorrhages
cotton-wool spots
edema of fundus
sequelae of CRVO: macular degeneration
glaucoma
Treatment of CRAO: thrombolysis of ophthalmic artery within 8hrs of symp onset
IV acetazolamide -decrease IOP - increase drainage of aqu. humor
sequelae of CRAO: untreated - retinal infarction, permanent blindness
Treatment of CRVO: laser photocoagulation - variable results
Estrogen functions (8): follicle growth
endometrial proliferation
myometrial excitability
hepatic synthesis of transport proteins
feedback inhibition of FSH
LH surge
smooth muscle relaxation
Progesterone functions (5): endometrial gland secretions
spiral artery development
decreased myometrial excitability
increased body temperature
inhibition of LH, FSH
hCG functions (2): maintians corpus luteum for T1 by acting like LH
detect pregnancy (in urine at 8 days)
physiologic changes in pregnancy - CVS (4): increased CO (30-50%), HR (10-15bpm), SV
possible S3, syst. murmurs (Normal) (new diast. murmur never normal!)
decreased SVR
decreased BP T1, normalizes by 40 weeks
cardiomeagly on CXR d/t heart displacement upwards
physiologic changes in pregnancy - cervix (2): softening and cyanosis ~4wks
bloody show = thick mucus clot
physiologic changes in pregnancy - endocrine (3): high estrogen => â†‘TBG, bound T3, T4, unchanged active unbound hormone
HPL - acts as insulin antagonist to maintain fetal glucose => prolonged post-prandial hyperglycemia, fasting hyperinsulinemia, triglyceridemia, exaggerated starvation ketone response
â†‘total and free cortisol
physiologic changes in pregnancy - GI (4): N/V (<=70%) resolves by 14-16wks
â†‘acid reflux d/t â†“LES tone
constipation d/t â†“bowel motility,â†‘H2O absorption
â†‘biliary cholesterol
physiologic changes in pregnancy - hematologic: â†‘plasma V (50%), RBC mass (30%)=> â†“Hb, hct = 'physiologic anemia'
WBC count â†‘s throughout X=10
pregnancy = hypercoagulable state
physiologic changes in pregnancy - pulmonary: â†‘tidal V (40%)
â†“TLC, RV,ERV
RR same
â†‘minute vent. => â†‘Pa/PAO2, â†“Pa/PACO2 = 'dyspnea of pregnancy'
physiologic changes in pregnancy - Renal: kidneys dilate
â†‘GFR (50%)
â†‘RPF (30%)
â†‘estrogen/progesterone => â†‘RAAS = â†‘aldosterone
physiologic changes in pregnancy - skin: â†‘estrogen - stigmata like liver disease
â†‘Î±MSH, steroids => hyperpigmentation - midline (linea nigra), face (chloasma), perineum
physiologic changes in pregnancy - vagina: thick acidic secretions
Chadwick's sign = violet colouration from â†‘blood flow
Nagle's rule = EDD: add 9m + 7d to 1st day of LMP
Ways to determine GA: uterine size
quickening (17-18wks)
fetal heart tones (10wks)
U/S fetal crown-rump length (5-12wks) biparietal diameter (20-30wks)
Labs at initial visit for pregnancy: CBC, UA + culture, Pap, blood type, Rh + Ab screen, rubella Ab titer, HBsAg, syphilis screen, cervical gonoccocal & chlamydia
PPD
glucose teting
HIV
Labs at 15-19wks GA: MSAFP or triple screen (=MSAFP, estiol, β-hCG)
amnio if >35y/o
Labs at 26-28wks GA: glucose loading test
give Rhogam at 28 wks if mom Rh-ve
Labs at 32-36wks GA: cerval chlamydia + gonorrhea in high risk
GBS screen
causes of â†‘MSAFP (MoM >2.5): 1. open NTD - anencephaly, SB
2. abdominal wall defects - gastroschisis, omphalocele
3. multiple gestation
4. incorrect dates
5. fetal death
6. placental abnormalities - abruption
causes of â†“MSAFP (MoM<0.5): need amnio and karyotyping to r/o chromosomal abnormalities
- trisomy 18, 21
pattern of triple screen with Down's: â†“AFP, estriol
â†‘hCG
pattern of triple screen with trisomy 18: â†“AFP, estriol, hCG
Compare complications of amnio with CVS: amnio (15-17wks)
fetal maternal hemorrhage 1-2%
fetal loss 0.5%
CVS (10-12wks)
fetal loss 1%
inability to Dx NTD
limb defects if <9wks GA
Indications for percutaneous umbilical blood sampling: Ax/Rx Rh isoimmunization/erythroblastosis fetalis
karyotyping
fetal infection (CMV, toxo, rubella)
genetic dz
fetal acid-base status
Normal labour and deliver stages: first
latent - onset to 3-4cm
active - 4cm to 10cm (1.2cm/h primi, 1.5cm/h
multip)increased with CPD
2nd - complete dilatation to delivery
34d - delivery of infant to placenta
Factors affecting active phase of labour: 3P's
power
passenger
pelvis
Normal NST: FHR monitored by doppler correlated with reported mvts by mom
- acceleration â‰¥15bpm above baseline for â‰¥15sec twice in 20min
positive contraction stress test: repetitive late decels during â‰¥3 contractions in 10min
Biophysical profile: "Test the Baby MAN" - give score of 0 or 2 for each
Tone
Breathing
Movement
Amniotic fluid volume
NST
"+ve test" = score 0-2
Early decelerations: begin and end with contraction
caused by cephalic compression (no fetal distress)
Variable decelerations: at any time during contraction
Caused by:
umbilical cord compression (change maternal position)
Late decelerations: begin at peak of contraction and end after contraction has finished
- uteroplacental insufficiency
- fetal hypoxemia
- potentially d/t abruption or hypotension
- if repetitive and severe deliver ASAP
Hyperemesis Gravidarum: intractable N/V after 14-16wks
poor wt gain/wt loss
more common in G1P0, molar pregnancies
labs - ketonemia, ketonuria, hyponatremia, hypokalemic-hypochloremic m.a.
Diagnosis of GDM: fasting serum glucose >126mg/dL
random >200mg/dL
abnormal GTT
1hr (50g) >140gm/dL
3hr (75g)with any 2 of -
fasting â‰¥95,
1h â‰¥180
2h â‰¥155
3h â‰¥140

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Number of cards 250