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264 Cards in this Set

  • Front
  • Back
what are the parasellar signs and sx
visual field changes
tx of prolactinoma
bromocriptine x 2 yrs prior to cessation
cabergoline (alternative da agonist)

surgery if no response to either tx
complications of acromegaly
cavernous sinus compression
sphenoid sinus invasion
how to dx acromegaly
elevated igf-1
oral glucose suppression test (glucose fails to suppress gh) = confirmatory test
origins of craniopharyngioma
from embryologic remnants of rathke's pouch
sx fo craniopharyngioma
vision changes
endocrine sx are related to whatever is secreted
what is the adh level in di
causes of central di
what can cause nephrogenic di
hypernatremia in di
only occurs is there is impaired thirst drive or no access to water
why is there no edema in siadh
natriuresis occurs from anp release secondary to volume overload --> na is excreted and raas is inhibited
tx of siadh
if mild (120-130) and asx: fluid restrition
if mod (110-120) and asx: NS + loop diuretic
if severe (sx): hypertonic saline +/- furosemide
tx of nephrogenic di
tx w hctz (works by depleting body of na --> reabsorption of na/water in prox tubules)
medical tx of hyperparathyroid
ca + vit d
when should surgery be done on pts with hyperpara
w sx
evidence of bone loss
ways (w h&p) to distinguish between iatrogenic cushings and actual cushings
no darkened skin and no androgen excess with iatrogenic
(steroid suppress androgen production by adrenals)
way to screen for primary hyperaldo
check plasma aldo: renin ratio
way to dx primary hyperaldo
saline infusion test (nml response is to see decreased aldo)
way to determine the cause of primary hyperaldo
adrenal venous sampling for aldo
if b/l, then due to hyperplasia
if u/l, then adenoma
if primmary hyperaldo is from hyperplasia - tx?
if primary hyperaldo is from adenoma -tx?
what is conn syndrome
aldo producing adenoma (#1 reason for hyperaldo)
primary adrenal insuff
adrenal problems b/c there is problem directly with adrenals (tb, idiopathic, autoimmune)
secondary adrenal insuff
from stopping steroids, hypopit
teritary adrenal insuff
from hypothal dz
when will you see hypoaldo associated with adrenal insuff (primary, secondary, tertiary)
how to differentiate between primary and secondary adrenal insuff
give iv infusion of acth
if there is no increase in plasma cortisolhtne is primary
if no increase after 1st infusion, but there is increase after multiple, then secondary b/c adrneal aren't used to being stimulated
findings on physical that would sugges malignant thyroid nodule
no mov't of nodule with swallowing
increased calcitonin
what type of thyroid lesions require lobectomy
cold nodules (there is increased risk of malignancy)
which type of thryoid ca produces calcitonin
medullary ca
orphan annie nuclei
papillary thyroid ca h
histologic findings of hashimoto's
dense lymphocytic infiltrate
histologic findings of grave's disease
follicular hyperplasia
pathophys of bartter's syndrome
polyuria, polydipsia, growth and mental retardation
defetive na and cl reabsorption --> hypovolemia --> raas activation --> hypokalemia and h+ secretion --> hypokalemic metabolic alkalosis

sx of osteomalacia
blurring of spine
low/nml ca
decreased po4
increased pth
why is there abnml lipid profile in hypothyroid
hypothyroid --> downregulation of ldl receptors so there is less absorption of ldl
initial tx of asx pt with paget's
no tx
tx when pt is sx with paget's
tx of hyponatremia
if 120-130, asx: fluid restriction
110-120, asx: ns + furosemide
sx: hypertonic saline +/- furosemide
side effect of ptu
differential for htn + spontaneous hypokalemia
primary hyperaldo
renovascu dz
distinguish with plasma renal activity (low in hyperaldo, high in renovasc)
ca that is associated with hashimoto's
lymphoma of thyroid
signs of lymphoma of thyroid
donut sign on ct
decreased radioactive i
in addition to chf, what else do pts with acromegaly suffer from
increased strokes
colon ca
renal failure (from htn and hyperglycemia)
adrenal failure
use of bb in pheo
contraindicated b/c alpha-1 receptors take over bv --> catastrophic increase in bp
bb should be started after a-1 blockade is successful
instead, labetolol can also be used (has alpha and beta properties)
what causes the exophthalmos in graves
lymphos attack eom and orbital fat --> edema, proliferation of fibroblasts, and gag deposition
what causes eye grittiness in grave's
increased corneal exposure and keratitis from inability to completely close eyelid over protruding eye
most common causes of hypopituitarism post-partum
sheehan's syndrome
lymphocytic hypophysitis
what role do steroids play in thyroid hormones
steroids decrease peripheral conversion of t4--> t3
this improves thyrotoxic states
inhibits adh effects on dct can be used as tx for siadh
what are the main substrates for gluconeo
management of ptu induced agranulocytosis
when pt develops a fever or signs of illness, immediately d/c agranulocytosis (if occurrring w.i 90 days of starting med)
measure granulocytes
if wbc <1000, d/c ptu permanently and give iv abx
tx of the physical findings in di
if there is hypotension, give ns . then switch to 1/2 ns after bp is normal
if no hypotension initially, then just give 1/2 ns
how to screen all individuals for dm if no risk factors

if risk factors?
fasting blood glucose (<126)

random blood glucose (>200)
sx of osteomalacia
bone pain/tenderness
hypocalcemia, hypophosphatemia
location of arterial insufficiency ulcers
at fingertips, not at pressure points
pathogen of obesity and dm ii
obesity incresaes plasma levels of ffa --> increased insulin resistance and decreaed glucose uptake

ffa in liver increases glucose production (ffa normally stimulates insulin release but in dm ii this doesn't occur) --> hyperglycemia
familial hypocalciruia wiht hypercalcemia
decreased ca in urine and increased serum ca
benign condition, resulting from decreased sensitivity to free calcium
cause for envelope shaped crystals in urine
ethylene glycol
signs of asa intoxication
anion gap metabolic acidosis + respiratory alkalosis
which parts of the lungs are affected in centrolobular emphysema?

upper lung zones

pathogenesis of chronci bronchitis
excess mucous production narrows airways
inflammation and scarring in airways --> increase in mucous glands
smooth muscle hyperplasia results --> obx
pathogenesis of emphysema
excess in elastase (made by polys ad macrophages) --> lung digestion
alpha 1 AT inhibits elastase
smoke increases # macrophages and polys and inhibits alpha 1 AT
there is also increased oxidative stress on lung by free radical production
what happens to the fev 1 in copd
tx for copd exacerbation
b2 agonist +/- anticholinergics *
systemic corticosteroids
+/- intubation

*not given in asthma exacerbation
tx of asthma exacerbation
b2 agonist
theophylline/IV Mg*
supplemental o2*
ABx (if severe infx suspecdted)
+/- intubation

(* not given in copd)
pathogenesis of bronchiectasis
permanent dilation and destruction of bronchial walls
cilia are damaged
impaired defense and drainage system precipitates the dz
etiology of bronchiectasis
airway obx
complications of bronchiectasis
chronic cough
hemoptysis (from ruptured bv near brochial wall surfaces)
recurrent and persistent pna
which lung malignancy is associated with pth-like hormone release
squamous cell (s"ca"mous cell)
which lung ca is associated with hypertrophic pulmonary osteoarthropathy
squamous cell
when should sputum cytology be done for lung ca evaluation
if it is a central lesion
when should a needle bx be done for lung ca evaluation
for peripheral lesion
what should be used to evaluate peripheral lung nodules
needle bx
what should be used to evaluate entral lung lesions
sputum cytology (or bronchoscope)
description of fluid from pleural effusion in a malignancy
bloody pleural effusion
description of a pleural effusion from empyema
frankly purulent fluid
description of a parapneumonnic effusion
pleural effusion + pna
ph <7.2
tx of uncomplicated parapneumonic
tx with abx

tx with chest tue drainage + streptokinase (to accelerate drainage), LOA if needed
tx of empyema
repeated drainage, if persists, do rib resection and open drainage
causes of tension ptx
findings on cxr in tension ptx
trachea shifts away from ptx
management of tension ptx
do not do cxr if suspected!
tx immediately with needle insertion
why is tension ptx a medical emergency
will die of decresaed co and hpoxemia
there is decreased bp from decreased cardiac filling capacity b/c of svc/ivc compression
findings on cxr in spontaneous ptx
trachea shifts towards ptx
managment of spontaneous ptx
if small and asx, no tx needed
if big and sx give o2 and place chest tube (allows lung to re-expand)
benign mesothelioma
not related to asbestos
good prognosis
pulmonary fibrosis findings on cxr
ground glass

high res ct shows fibrosis best
pathogenesis of ild
inflammation of alveolar wall (from incresaed fibroelastic proliferation and collagen deposits) --> fibrosis, impaired gas exchange
lab findings in sarcoidosis
increased ace
hypercalcemia (from increased 1-alpha hydroxylase made by granulomas)
management of sarcoidosis
most cases resolve w/i 2 yrs and don't require tx
if sx are severe tx with steroids
histiocytosis x
chronic interstitial pna from abnormal proliferation of histiocytes
--> spontaneous ptx, lytic bone lesions, di
management of histiocytosis x
lung transplant may be necessary
differences between simple and complex coal workers pneumoconiosis
simple has no respiratory disability
complex --> fibrosis
consequences of asbestosis
increased risk of bronchogenic ca and malignant mesothelioma
cxr of asbestosis
hazy infiltrates with bilateral linear opacities
silicosis has increased risk of what other pulmonary dz
si/sx of berylliosis
diffuse pneumonitis, simmilar to sarcoidosis
there are granulomas
hypercalcemia, skin lesions
management of berylliosis
what type of hypersensitivity reaction is goodpasture's dz
type ii (igg vs glomerular and alveolar bm)
sx of goodpasture's dz
hemorrhagic pneumonitis and glomerulonephritis
management of goodpastures dz
effect of severe hypercapnia on brain
--> dyspnea and vasodilation of cerebral bv --> increased icp and impaired consciousness/coma
pathophysiology of hypoxemic respiratory failure vs hypercarbic respiratory failure
hypoxemic is from vv/q mismatch (either intrapulmonary shunt or decreased ventilation)
hypercarbic is from underlying lung dz or impaired ventilation
what are the 2 types of respiratory failure
pathophys of ards
diffuse inflammatory process from poly's activation in systemic/pulm circulation
--> massive intrapulmonary shunting that won't improve on 100% o2 (the shunting is from widespread atelectasis and collapse of alveoli, and surfactant dysfunction)
what is the best measurement to dx ards
pcwp, it is <18 in ards and >18 in pulmonary edema
different causes of pulmonary htn
obliterative (restricted to flow through small pulm bv, secondary to fibrosis)
vasoconstrictive (hypoxia induced vasoconstriction)
increased intrathoracic pressure (from ventilators)
primary pulm htn
pathogenesis of primary pulmonary htn
no heart or lung dz, but there is an abnml increase in pulmonary arteriolar restriction --> thickening of arteriolar walls --> worsening htn --> increased thickening of walls --> etc
dx of primary pulm htn
cardiac cath
cxr shows enlarged pulm arteries
big rv
clear lung fields
restrictive pft patterns
tx of primary pulmonary htn
pulmonary vasodilation (prostacyclins, ccbs)
they decrease pulmonary vascular resistance
what does pcwp measure
pulmonary artery pressure
la pressure
rv pressure
definition of solitary pulmonary nodule
completely surrounded by lung parenchyma
no contact with hilum, pleura, or mediastinum
doubling time for solitary pulmonary nodule if benign?
>1.5 yrs benign
>30 days infectious
in between: malignant
cxr: hemothorax
looks like pleural effusion
how do kidneys compensate for respiratory acidosis
kidneys increase hco3 retention and decrease cl reabsorption
theophylline toxicity
acts as a cns stimulants (ha, insomnia), n/v, arrhythmia from pshopodiesterase inhibition
adenosine antagonist increasing epi release
clinical sx of hemothorax
absent breath sounds
dullness to percussion
significant hypotension secondary to massive bleeding and traumatic laceration of lung parenchyma or damage to internal mammary arteries or intercostal artery
where is mesothelioma located in the lungs
the pleura
how much hco3 is retained for every increase of 1 in hco3
1 hco3 is retained for every 1 increase in co2
physical findings in lung consolidation
dullness to percussion
increased femitus
increaed bronchophony
increaesd egophony
increased whispered pectoriloquy
which malignancyies --> the majority of all pleural effusions
lung, breast ca, lymphomas
what is the first step in determining the cause of a pleural effusion
how does ppv affect intrathroacic pressure, ra pressure and vr

consequences of these changes

sudden loss of vr --> acute circulatory failure and death
mobile cavitary mass in lung
present wth intermittent hemoptysis
fungus ball forms b/c there is destruction of underlying pulmonary parenchyma
debris and hyphae coalesce
criteria for administration of supplemental o2
SaO2 <88%
Hct <55%
evidence of cor pulmonale
what is hypertrophic pulmonary osteoarthropathy

what does it represent
digital clubbing associated with sudden onset of arthropathy of wrists and hands secondary to underlying lung dz (ca, tb, etc)

= malignancy, esp in a pt w long-standing copd
hypertrophic osteoarthropathy
arthropathy of wrists and hands
sx flail chest
rib fx, lung field opacification, and severe tachypnea with respiratory distress after acute thoracic trauma

pts take shallow breasths and compensate for hypoxemia with increased rr

paradoxical chest movement possible
pathophysiology of how chf --> pulmonary edema
chf --> decreased co --> increased hydrostatic pressure in pulmonary vasc --> fluid leaves pulmonary capillaries into alveolar spaces --> pulmonary edema and pleural effusions

the pleural fluid is transudative
protein ratio <.5
ldh ratio <.6
>2/3 top normal ldh
tx of empyema
removal of fibrous peel surrounding empyema (abx won't penetrate)
pathogen of hemoptysis in bronchiectasis
rupture of bronchial arteries that have hypertrophied during the development of the dz
when to suspect legionella pna

what does cxr look like
in pts with no response to beta-lactams for cap
acute onset, fever, malaise, ha, and nonproductive cough common
--> confusion and severe ha, abdominal pain

there is patchy interstitial inflammation --> lobar consolidation over a few days
cxr findings of pulmonary contusion
may initially be negative
clinical sx of pulmonary contusion
several hours following the injury, hypoxia and respiratory distress result as pulmonary edema sets in

ivf will worsen sx
what role to calf veins play in dvts
they are a common site of dvt formation, but they rarely lead to sx
most common location of dvts
iliac, femoral
pathophysiology of ptx secondary to copd
alveolar sac destruction and formationof large airspaces --> ptx
when to suspect ptx in pts with copd
catastrophic worsening of sx
clinical sx of a copd exacerbation
increase in purulent sutum, rhonchi, wheezing
what should you think of if there is recurrent pna in same region of the lung

what test should you order
bronchial obx or possible bronchiogenic ca
must check ct of chest
causes of subcutaneous asthma
ptx (cxr)
tracheobronchial rupture (seen in trauma) - check bronchoscopy
side effects of b2 agonists
drives k into cells --> muscle weakness, arrrhythmias, ekg changes, tremor, ha, palpitations
what effect do glucocorticoids have on wbcs
they can induce neutrophilia and decrease eosinophils
lymphos are decreased
#1 danger of massive hemoptysis

asphixiation from airway flodding with blood

bronchoscopy to control bleeding and keep airway open
which pna is associated with erythma multiforme
m. pneumo
what happens to dlco in emphysema

in bronchitis

classic finding wiht klebsiella pna
currant jelly sputum
causes for acalculous cholecystitis
prolonged tpn/fasting
mechanical ventilation
how does the elevation of lfts affect tx for chronic hep b
tx will likely only be effective if the ast and alt are >2x the normal, otherwise the meds will likely not work
best way to stop acute variceal bleeding
is a solitary liver mass more likely to be from mets or primary malig
how to dx pancreatic ca
why is there increased estrogen in chronic liver dz
increased portosystemic shunting --> decreased sbg synthesis by liver, thereby increasing circulating estrogens
lfts in hepatic adenoma
usually normal
tx of cholangitis
IV ABx and ercp
what type of shock can be seen in pancreatitis
hypovolemic... secondary to increased vascular permeability from inflammation
what type of bili is in excess in dubin johnson syndrome
what type of bili is in excess in rotor's syndrome
what type of bili is elevated in gilbert's dz
what type of bili is elevated in crigler najjar
tx for hcv
ribavarin and interferon
tx for hbv
lamividine and interferon
how to dx angiodysplasia in gi tract
bleeding usually stops spontaneously, but if it doesn't, can use colonoscopy to coagulate
what deficiency can develop from carcinoid syndrome
niacin deficiency b/c there is increased formation of 5hiia from tryptophan, which requires niacin for synthesis
sx of niacin deficiency
where does carcinoid tumor metastasize to
liver, b/c liver can break down 5ht --> 5hiaa
what in stool sample is diagnostic for malabsorption
>7g fat/day
what do recurrent peptic ulcers + hypercalcemia make you think of
men i
(parathyroid adenoma, pancreatic tumor, papillary ca)
how to manage minimal rectal bleeding (blood on tp)
just do anoscopy
what are the types of ischemic strokes
which is most common
presentation of thrombotic stroke
pt wakes up with neuro deficits
presentation of embolic stroke
defecits are apparent immediately
presentation of lacunar strokes
very focal findings
pathophys of embolic stroke
most frequently, clots are thrown from heart
which bv in brain is most commonly affected in embolic stroke
pathopys of thrombotic stroke
usually from atherosclerotic plaque buildup in arteries (most commonly the mca)
pathophys of lacunar stroke
small bvs in brain affected, there is a narrowed arterial lumen from thickening of bv wall
which bv are affected in lacunar stroke
vessels of cow, basilar or vertebral system
which bv is most commonly involved in thrombotic stroke
how to dx ischemic stroke
first get ct s contrast to r/o hemorrhagic stroke
ischemic strokes are dark on ct
hemorrhagic strokes are bright
complications of ischemic stroke
cerebral edema w/i 1-2 days, maximal mass effect by day 10
how to manage a ct-diagnosed ischemic stroke
if <3 hrs have elapsed since the onset of sx, then give tpa
if time unknown or >3hr don't give at all

start asa w/i 24 hrs (unless tpa has been given)
do NOT give anticoag
keep pt NPO until airway has been evaluated
what are the indications for anti-hypertensives in pts with ischemic strokes
don't give unless:
1. BP >220/120 or >185/110 if on tpa
2. there is a life threatening medical emergecny requiring bp be lowered (dissection, etc)
when should cea be performed
when pt has sx and is >70% stenotic
describe presentation of ich
abrupt onset of focal neuro defects that worsen over 30-90 mins
altered levels of consciousness
mortality rate of hemorrhagic strokes
50% at 30 days
major complication of ich
hematomas can form --> increased icp
etiology of ich
htn (esp if sudden increase in bp) --> rupture of small bv in brain parenchyma

chronic htn --> degeneration of small arteries --> microaneurysms rupture
most common locations for ich
basal ganglia > pons > cbl
tx of ich
decrease bp if >160/105
use mannitol if increased icp
no steroids
when is surgery indicated for ich
when there is a cbl hematoma
clinical presenatation of sah
"worst headache of my life"
--> loc, n/v, meningeal irritation
pathophysiology of sah
ruptured berry aneurysm
how to dx sah
ct will id 90% of sah, but if clinical suspicion is high and the ct is negative, do lp (look for xanthochromia)
management once sah is diagnosed
cerebral angiography to detect site of rupture, so it can be surgically clipped

gradually decrease bp (htn may be compensating for decreased cerebral perfusion)
complications of sah

both of which --> ischemia, infarction, sz, siadh
how can vasospasm be managed
give nifedipine, it reduces cerebral infarction by 1/3
first meds that should be started in parkinsons
da receptor agonists - they can delay the need for levadopa
start as soon as diagnosis is established
what role does amantadine play in parkinsons
transiently improves sx
side effects of levodopa-carvidopa
dyskinesias after 5-7 yrs of tx
what role does selegiline play in parkinson's
reduces the metabolism of levodopa
early presentation of huntinton's dz
altered behavior
personality changes
antisocial behaviors
features of essential tremor
exacerbated by intentional movement
decreased by etoh
tx of essential tremor
features of parkinson's tremor
worst at rest, better with movement
features of a cbl tremor
ataxia also present
tremor is better with rest
friedrich's ataxia
impaired vibratory sense/proprioception
pathologic findings in alzheimers
senile plaques
neurofibrillary tangles
what do imaging studies show in alzheimers
cortical atrophy and enlarged ventricles
tx of alzheimers
no cure, but can give ache inhibitors (donepezil)
vit e?
features of lewy body dementia
alzheimer and parkinsons' features
visual hallucinations + eps
change in ms
tx of lewy body dementia
moa of selegilien
mao-b inhibitor
persistent vegitative state
unresponsive but eyes open, limbs randomly move
can't dc life support
tx for acute attacks of ms
high dose iv steroids
long term management for ms
baclofen for spasticity
presentation of guillan barre syndrome
rapidly evolving, ascending weakness and paralysis in all 4 extremities (usually symmetric)
what is usually spared in aidp
sphincter control and ms
what does csf show on aidp
increased protein
nml cell count
tx of aidp
presentation of cidp
more slowly evolving than aidp
can be associated with systemic illness
tx of cidp
steroids (usually for years)
what is the most common neoplasm in the brain
features of astrocytoma
can cross corpus callosum
located in hemisphere
examples of astrocytomas tumors
anaplastic astrocytoma
low grade astrocytoma
what does "ring enhancing lesion" seen on mri actually mean
enhancing tissue with a non-enhancing necrotic center
pathology of gbm
pseudopalisading cells
pathology of oligodendroglioma
fried egg appearance
pathophys of myasthenia gravis
ab against nicotinic receptors at neuromuscular jxn
where are nicotinic receptors located in the body
they act as all of the presynaptic receptors for every type of nerve transmission
what should be done after dx of myasthenia gravis has been made
check ct for thymoma
tx for myasthenia gravis
tx with ache inhibitors
clinical features of lambert-eaton myasthenic syndrome
diffeent from mg b/c weakness actually improves with movement, instead of worsens b/c of it

proximal muscle weakness and areflexia
what ca is lambert-eaton associated with
pathophys of lambert eaton syndrome
ab vs ca channels
sx of syringomyelia
bilateral loss of pain and temperature over the shoulders (in a cape-like distribution) --> preserved touch
there is muscle atrophy in the hands
sx of brown-sequard syndrome
contralateral spinothalamic sx
ipsilateral corticospinal tracts and dorsal column tracts affected
where are lesions in peripheral vertigo
cochlea or retrocochlear areas
there are no brainstem features
sx of benign positional vertigo
vertigo in specific rotations or positions
abrupt onset
recovery is usually complete
sx of meniere's dz
hearing loss
attacks last for hrs - days
hearing loss can become permanent
what feature on physical exam is important to note b/c it is present in central vertigo but not in peripheral
vertical nystagmus
sx taht become refractory with repetitive movements are suggestive of peripheral vertigo
there are also brainstem sx in central vertigo
etiologies of peripheral vertigo
meniere's dz
accoustic neuromas
etiologies of central vertigo
vertibro-basilar insufficiency
dx of vasovagal
can do tilt-table test but should wait until there have been at least 2 episodes of syncope
tx of orthostatic syncope
increased na intake, increased fluids
+/- fludrocortisone
tx of vasovagal syncope
beta blockers
clinical features of als
umn and lmn lesions
motor system ONLY is affected
there are no sensory deficits
bowel and bladder fxn remain unaffected
cognition intact
tx of als
riluzole can delay death by 3-5 months
tx of trigeminal neuralgia
tx with carbemazepine
course of trigeminal neuralgia
has a relapsing, remitting course
what does cerebral perfusion pressure (cpp) =
cpp = mabp - icp
what relationship is there between jvp and icp
if jvp is elevated then the csf can't get reabsorbed so icp gets elevated
what causes vasoconstriction in the barin
clinical features of juvenile myoclonic epilepsy
there is a nml neuro exam and nml development
sz are brief b/l arm and leg jerks, loc, fall to floor, then rhythmic jerking of whole body for 2-3 mins
features of frontotemporal dementia
personality changes, loss of initiative, slowing of thought, preserved recent memory
clinical features of spinal muscular atrophy
no sensory abnormalities
--> symmetric proximal muscle weakness and atrophy
clinical features of charcot marie tooth dz
distal muscle atrophy
sensory loss
hammer toes
pathophys of cervical spondylosis
chronic d/o of degenerative and hypertrophic changes of vertebral ligaments and disks
--> narrowed spinal cord canal --> compression
what anti-epileptic drugs are best tolerated in elderly
clinical features of vasculitic neuropathy
acute onset of asymmetric weakness and sensory loss and severe pain
who gets vasculitic neuropathy
other vasculitides
clinical features of paroxysmal hemicrania
unilateral headache of seconds to minutes in duration
these ha are disabling
tx of paroxysmal hemicrania