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264 Cards in this Set
- Front
- Back
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what are the parasellar signs and sx
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visual field changes
ha |
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tx of prolactinoma
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bromocriptine x 2 yrs prior to cessation
cabergoline (alternative da agonist) surgery if no response to either tx |
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complications of acromegaly
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cavernous sinus compression
sphenoid sinus invasion |
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how to dx acromegaly
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elevated igf-1
oral glucose suppression test (glucose fails to suppress gh) = confirmatory test |
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origins of craniopharyngioma
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from embryologic remnants of rathke's pouch
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sx fo craniopharyngioma
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papilledema
ha vision changes endocrine sx are related to whatever is secreted |
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what is the adh level in di
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low
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causes of central di
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sarcoid
tb syphilis |
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what can cause nephrogenic di
|
li
hypokalemia hypercalcemia |
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hypernatremia in di
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only occurs is there is impaired thirst drive or no access to water
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why is there no edema in siadh
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natriuresis occurs from anp release secondary to volume overload --> na is excreted and raas is inhibited
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tx of siadh
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if mild (120-130) and asx: fluid restrition
if mod (110-120) and asx: NS + loop diuretic if severe (sx): hypertonic saline +/- furosemide |
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tx of nephrogenic di
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tx w hctz (works by depleting body of na --> reabsorption of na/water in prox tubules)
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medical tx of hyperparathyroid
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ca + vit d
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when should surgery be done on pts with hyperpara
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<50
w sx evidence of bone loss |
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ways (w h&p) to distinguish between iatrogenic cushings and actual cushings
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no darkened skin and no androgen excess with iatrogenic
(steroid suppress androgen production by adrenals) |
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way to screen for primary hyperaldo
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check plasma aldo: renin ratio
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way to dx primary hyperaldo
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saline infusion test (nml response is to see decreased aldo)
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way to determine the cause of primary hyperaldo
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adrenal venous sampling for aldo
if b/l, then due to hyperplasia if u/l, then adenoma |
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if primmary hyperaldo is from hyperplasia - tx?
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spironolactone
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if primary hyperaldo is from adenoma -tx?
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surgery
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what is conn syndrome
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aldo producing adenoma (#1 reason for hyperaldo)
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primary adrenal insuff
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adrenal problems b/c there is problem directly with adrenals (tb, idiopathic, autoimmune)
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secondary adrenal insuff
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from stopping steroids, hypopit
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teritary adrenal insuff
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from hypothal dz
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when will you see hypoaldo associated with adrenal insuff (primary, secondary, tertiary)
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primary
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how to differentiate between primary and secondary adrenal insuff
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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 |
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findings on physical that would sugges malignant thyroid nodule
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no mov't of nodule with swallowing
firm irregular increased calcitonin |
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what type of thyroid lesions require lobectomy
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cold nodules (there is increased risk of malignancy)
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which type of thryoid ca produces calcitonin
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medullary ca
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orphan annie nuclei
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papillary thyroid ca h
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histologic findings of hashimoto's
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dense lymphocytic infiltrate
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histologic findings of grave's disease
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follicular hyperplasia
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pathophys of bartter's syndrome
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polyuria, polydipsia, growth and mental retardation
defetive na and cl reabsorption --> hypovolemia --> raas activation --> hypokalemia and h+ secretion --> hypokalemic metabolic alkalosis normotensive |
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sx of osteomalacia
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pseudofx
blurring of spine low/nml ca decreased po4 increased pth |
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why is there abnml lipid profile in hypothyroid
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hypothyroid --> downregulation of ldl receptors so there is less absorption of ldl
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initial tx of asx pt with paget's
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no tx
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tx when pt is sx with paget's
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bisphosphonates
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tx of hyponatremia
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if 120-130, asx: fluid restriction
110-120, asx: ns + furosemide sx: hypertonic saline +/- furosemide |
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side effect of ptu
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agranulocytosis
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differential for htn + spontaneous hypokalemia
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primary hyperaldo
renovascu dz distinguish with plasma renal activity (low in hyperaldo, high in renovasc) |
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ca that is associated with hashimoto's
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lymphoma of thyroid
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signs of lymphoma of thyroid
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donut sign on ct
decreased radioactive i |
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in addition to chf, what else do pts with acromegaly suffer from
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increased strokes
colon ca renal failure (from htn and hyperglycemia) adrenal failure |
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use of bb in pheo
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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) |
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what causes the exophthalmos in graves
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lymphos attack eom and orbital fat --> edema, proliferation of fibroblasts, and gag deposition
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what causes eye grittiness in grave's
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increased corneal exposure and keratitis from inability to completely close eyelid over protruding eye
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most common causes of hypopituitarism post-partum
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sheehan's syndrome
lymphocytic hypophysitis |
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what role do steroids play in thyroid hormones
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steroids decrease peripheral conversion of t4--> t3
this improves thyrotoxic states |
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demecloscycline
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inhibits adh effects on dct can be used as tx for siadh
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what are the main substrates for gluconeo
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ala
lactate glycerol |
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management of ptu induced agranulocytosis
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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 |
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tx of the physical findings in di
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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 |
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how to screen all individuals for dm if no risk factors
if risk factors? |
fasting blood glucose (<126)
random blood glucose (>200) |
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sx of osteomalacia
labs |
bone pain/tenderness
hypocalcemia, hypophosphatemia |
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location of arterial insufficiency ulcers
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at fingertips, not at pressure points
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pathogen of obesity and dm ii
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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 |
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familial hypocalciruia wiht hypercalcemia
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decreased ca in urine and increased serum ca
benign condition, resulting from decreased sensitivity to free calcium |
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cause for envelope shaped crystals in urine
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ethylene glycol
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signs of asa intoxication
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fever
tinnitus tachypnea anion gap metabolic acidosis + respiratory alkalosis |
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which parts of the lungs are affected in centrolobular emphysema?
panlobular |
upper lung zones
bases |
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pathogenesis of chronci bronchitis
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excess mucous production narrows airways
inflammation and scarring in airways --> increase in mucous glands smooth muscle hyperplasia results --> obx |
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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 |
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what happens to the fev 1 in copd
fev1/fvc? |
decreased
decreased |
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tx for copd exacerbation
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b2 agonist +/- anticholinergics *
systemic corticosteroids abx ppv* +/- intubation *not given in asthma exacerbation |
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tx of asthma exacerbation
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b2 agonist
steroids theophylline/IV Mg* supplemental o2* ABx (if severe infx suspecdted) +/- intubation (* not given in copd) |
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pathogenesis of bronchiectasis
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permanent dilation and destruction of bronchial walls
cilia are damaged impaired defense and drainage system precipitates the dz |
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etiology of bronchiectasis
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cff
immunodeficiency airway obx |
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complications of bronchiectasis
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chronic cough
hemoptysis (from ruptured bv near brochial wall surfaces) recurrent and persistent pna |
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which lung malignancy is associated with pth-like hormone release
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squamous cell (s"ca"mous cell)
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which lung ca is associated with hypertrophic pulmonary osteoarthropathy
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adenoca
squamous cell |
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when should sputum cytology be done for lung ca evaluation
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if it is a central lesion
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when should a needle bx be done for lung ca evaluation
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for peripheral lesion
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what should be used to evaluate peripheral lung nodules
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needle bx
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what should be used to evaluate entral lung lesions
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sputum cytology (or bronchoscope)
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description of fluid from pleural effusion in a malignancy
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bloody pleural effusion
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description of a pleural effusion from empyema
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frankly purulent fluid
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description of a parapneumonnic effusion
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pleural effusion + pna
ph <7.2 |
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tx of uncomplicated parapneumonic
complicated |
tx with abx
tx with chest tue drainage + streptokinase (to accelerate drainage), LOA if needed |
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tx of empyema
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repeated drainage, if persists, do rib resection and open drainage
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causes of tension ptx
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cpr
barotrauma trauma |
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findings on cxr in tension ptx
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trachea shifts away from ptx
DON'T DO CXR IF SUSPECTED! TREAT FIRST! |
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management of tension ptx
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do not do cxr if suspected!
tx immediately with needle insertion |
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why is tension ptx a medical emergency
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will die of decresaed co and hpoxemia
there is decreased bp from decreased cardiac filling capacity b/c of svc/ivc compression |
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findings on cxr in spontaneous ptx
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trachea shifts towards ptx
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managment of spontaneous ptx
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if small and asx, no tx needed
if big and sx give o2 and place chest tube (allows lung to re-expand) |
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benign mesothelioma
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not related to asbestos
good prognosis |
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pulmonary fibrosis findings on cxr
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reticular
reticulonodular ground glass honeycombing high res ct shows fibrosis best |
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pathogenesis of ild
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inflammation of alveolar wall (from incresaed fibroelastic proliferation and collagen deposits) --> fibrosis, impaired gas exchange
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lab findings in sarcoidosis
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increased ace
hypercalcemia (from increased 1-alpha hydroxylase made by granulomas) |
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management of sarcoidosis
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most cases resolve w/i 2 yrs and don't require tx
if sx are severe tx with steroids |
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histiocytosis x
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chronic interstitial pna from abnormal proliferation of histiocytes
--> spontaneous ptx, lytic bone lesions, di |
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management of histiocytosis x
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steriods
lung transplant may be necessary |
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differences between simple and complex coal workers pneumoconiosis
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simple has no respiratory disability
complex --> fibrosis |
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consequences of asbestosis
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increased risk of bronchogenic ca and malignant mesothelioma
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cxr of asbestosis
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hazy infiltrates with bilateral linear opacities
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silicosis has increased risk of what other pulmonary dz
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tb!
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si/sx of berylliosis
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diffuse pneumonitis, simmilar to sarcoidosis
there are granulomas hypercalcemia, skin lesions |
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management of berylliosis
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steroids
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what type of hypersensitivity reaction is goodpasture's dz
|
type ii (igg vs glomerular and alveolar bm)
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sx of goodpasture's dz
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hemorrhagic pneumonitis and glomerulonephritis
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management of goodpastures dz
|
plasmapheresis
cyclophosphamide steroids |
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effect of severe hypercapnia on brain
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--> dyspnea and vasodilation of cerebral bv --> increased icp and impaired consciousness/coma
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pathophysiology of hypoxemic respiratory failure vs hypercarbic respiratory failure
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hypoxemic is from vv/q mismatch (either intrapulmonary shunt or decreased ventilation)
hypercarbic is from underlying lung dz or impaired ventilation |
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what are the 2 types of respiratory failure
|
hypoxemic
hypercarbic |
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pathophys of ards
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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) |
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what is the best measurement to dx ards
|
pcwp, it is <18 in ards and >18 in pulmonary edema
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different causes of pulmonary htn
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obliterative (restricted to flow through small pulm bv, secondary to fibrosis)
vasoconstrictive (hypoxia induced vasoconstriction) increased intrathoracic pressure (from ventilators) primary pulm htn |
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pathogenesis of primary pulmonary htn
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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
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dx of primary pulm htn
|
cardiac cath
cxr shows enlarged pulm arteries big rv clear lung fields restrictive pft patterns |
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tx of primary pulmonary htn
|
pulmonary vasodilation (prostacyclins, ccbs)
they decrease pulmonary vascular resistance |
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what does pcwp measure
pulmonary artery pressure |
la pressure
rv pressure |
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definition of solitary pulmonary nodule
|
<3cm
completely surrounded by lung parenchyma no contact with hilum, pleura, or mediastinum |
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doubling time for solitary pulmonary nodule if benign?
malignant? |
>1.5 yrs benign
>30 days infectious in between: malignant |
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cxr: hemothorax
|
looks like pleural effusion
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how do kidneys compensate for respiratory acidosis
|
kidneys increase hco3 retention and decrease cl reabsorption
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theophylline toxicity
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acts as a cns stimulants (ha, insomnia), n/v, arrhythmia from pshopodiesterase inhibition
adenosine antagonist increasing epi release |
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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 |
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where is mesothelioma located in the lungs
|
the pleura
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how much hco3 is retained for every increase of 1 in hco3
|
1 hco3 is retained for every 1 increase in co2
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physical findings in lung consolidation
|
dullness to percussion
increased femitus increaed bronchophony increaesd egophony increased whispered pectoriloquy |
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which malignancyies --> the majority of all pleural effusions
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lung, breast ca, lymphomas
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what is the first step in determining the cause of a pleural effusion
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thoracocentesis
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how does ppv affect intrathroacic pressure, ra pressure and vr
consequences of these changes |
increases
incresaes decreases sudden loss of vr --> acute circulatory failure and death |
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aspergilloma
|
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 |
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criteria for administration of supplemental o2
|
pa02<55
SaO2 <88% Hct <55% evidence of cor pulmonale |
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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 |
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hypertrophic osteoarthropathy
|
arthropathy of wrists and hands
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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 |
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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 |
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tx of empyema
|
removal of fibrous peel surrounding empyema (abx won't penetrate)
|
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pathogen of hemoptysis in bronchiectasis
|
rupture of bronchial arteries that have hypertrophied during the development of the dz
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|
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 |
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|
cxr findings of pulmonary contusion
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may initially be negative
|
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clinical sx of pulmonary contusion
|
several hours following the injury, hypoxia and respiratory distress result as pulmonary edema sets in
ivf will worsen sx |
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what role to calf veins play in dvts
|
they are a common site of dvt formation, but they rarely lead to sx
|
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most common location of dvts
|
iliac, femoral
popliteal |
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pathophysiology of ptx secondary to copd
|
alveolar sac destruction and formationof large airspaces --> ptx
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when to suspect ptx in pts with copd
|
catastrophic worsening of sx
|
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clinical sx of a copd exacerbation
|
increase in purulent sutum, rhonchi, wheezing
|
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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
|
|
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what effect do glucocorticoids have on wbcs
|
they can induce neutrophilia and decrease eosinophils
lymphos are decreased |
|
|
#1 danger of massive hemoptysis
tx |
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 |
decreased
nml |
|
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classic finding wiht klebsiella pna
|
currant jelly sputum
|
|
|
causes for acalculous cholecystitis
|
burns
trauma prolonged tpn/fasting mechanical ventilation ischemia |
|
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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
|
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best way to stop acute variceal bleeding
|
sclerotherapy
|
|
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is a solitary liver mass more likely to be from mets or primary malig
|
mets
|
|
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how to dx pancreatic ca
|
ct
|
|
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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
|
conjugated
|
|
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what type of bili is in excess in rotor's syndrome
|
conjugated
|
|
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what type of bili is elevated in gilbert's dz
|
unconjugated
|
|
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what type of bili is elevated in crigler najjar
|
unconjugated
|
|
|
tx for hcv
|
ribavarin and interferon
|
|
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tx for hbv
|
lamividine and interferon
|
|
|
how to dx angiodysplasia in gi tract
|
colonoscopy
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
|
dementia
dermatitis diarrhea |
|
|
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 |
thrombotic
embolic* lacunar tia |
|
|
presentation of thrombotic stroke
|
pt wakes up with neuro deficits
|
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presentation of embolic stroke
|
defecits are apparent immediately
|
|
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presentation of lacunar strokes
|
very focal findings
|
|
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pathophys of embolic stroke
|
most frequently, clots are thrown from heart
|
|
|
which bv in brain is most commonly affected in embolic stroke
|
mca
|
|
|
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
|
mca
|
|
|
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
|
sz
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 NITROPRUSSIDE use mannitol if increased icp no steroids |
|
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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
PCA > ACA > MCA |
|
|
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
|
rerupture
vasospasm 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
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transiently improves sx
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side effects of levodopa-carvidopa
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dyskinesias after 5-7 yrs of tx
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what role does selegiline play in parkinson's
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reduces the metabolism of levodopa
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early presentation of huntinton's dz
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altered behavior
irritability personality changes antisocial behaviors |
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features of essential tremor
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exacerbated by intentional movement
decreased by etoh |
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tx of essential tremor
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propranolol
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features of parkinson's tremor
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worst at rest, better with movement
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features of a cbl tremor
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coarse
ataxia also present nystagmus dysarthria tremor is better with rest |
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friedrich's ataxia
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ataxia
nystagmus impaired vibratory sense/proprioception |
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pathologic findings in alzheimers
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senile plaques
neurofibrillary tangles |
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what do imaging studies show in alzheimers
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cortical atrophy and enlarged ventricles
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tx of alzheimers
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no cure, but can give ache inhibitors (donepezil)
vit e? |
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features of lewy body dementia
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alzheimer and parkinsons' features
visual hallucinations + eps change in ms |
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tx of lewy body dementia
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antipsychotics
selegeline |
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moa of selegilien
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mao-b inhibitor
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persistent vegitative state
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unresponsive but eyes open, limbs randomly move
can't dc life support |
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tx for acute attacks of ms
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high dose iv steroids
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long term management for ms
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ifn
immunosuppressives baclofen for spasticity |
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presentation of guillan barre syndrome
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rapidly evolving, ascending weakness and paralysis in all 4 extremities (usually symmetric)
areflexia |
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what is usually spared in aidp
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sphincter control and ms
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what does csf show on aidp
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increased protein
nml cell count |
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tx of aidp
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ivig/plasmapheresis
DO NOT GIVE STEROIDS |
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presentation of cidp
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more slowly evolving than aidp
can be associated with systemic illness |
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tx of cidp
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steroids (usually for years)
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what is the most common neoplasm in the brain
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astrocytoma
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features of astrocytoma
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can cross corpus callosum
located in hemisphere |
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examples of astrocytomas tumors
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gbm
anaplastic astrocytoma low grade astrocytoma oligodendroglioma ependymoma |
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what does "ring enhancing lesion" seen on mri actually mean
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enhancing tissue with a non-enhancing necrotic center
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pathology of gbm
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pseudopalisading cells
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pathology of oligodendroglioma
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fried egg appearance
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pathophys of myasthenia gravis
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ab against nicotinic receptors at neuromuscular jxn
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where are nicotinic receptors located in the body
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they act as all of the presynaptic receptors for every type of nerve transmission
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what should be done after dx of myasthenia gravis has been made
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check ct for thymoma
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tx for myasthenia gravis
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tx with ache inhibitors
thymectomy immunosuppression plasmapheresis |
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clinical features of lambert-eaton myasthenic syndrome
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diffeent from mg b/c weakness actually improves with movement, instead of worsens b/c of it
proximal muscle weakness and areflexia |
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what ca is lambert-eaton associated with
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sclc
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pathophys of lambert eaton syndrome
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ab vs ca channels
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sx of syringomyelia
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bilateral loss of pain and temperature over the shoulders (in a cape-like distribution) --> preserved touch
there is muscle atrophy in the hands |
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sx of brown-sequard syndrome
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contralateral spinothalamic sx
ipsilateral corticospinal tracts and dorsal column tracts affected |
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where are lesions in peripheral vertigo
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cochlea or retrocochlear areas
there are no brainstem features |
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sx of benign positional vertigo
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vertigo in specific rotations or positions
abrupt onset recovery is usually complete |
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sx of meniere's dz
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vertigo
tinnitus hearing loss attacks last for hrs - days hearing loss can become permanent |
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what feature on physical exam is important to note b/c it is present in central vertigo but not in peripheral
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vertical nystagmus
sx taht become refractory with repetitive movements are suggestive of peripheral vertigo there are also brainstem sx in central vertigo |
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etiologies of peripheral vertigo
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meniere's dz
bpv drugs accoustic neuromas |
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etiologies of central vertigo
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ms
vertibro-basilar insufficiency migraine |
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dx of vasovagal
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can do tilt-table test but should wait until there have been at least 2 episodes of syncope
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tx of orthostatic syncope
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increased na intake, increased fluids
+/- fludrocortisone |
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tx of vasovagal syncope
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beta blockers
disopyramidine |
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clinical features of als
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umn and lmn lesions
motor system ONLY is affected there are no sensory deficits bowel and bladder fxn remain unaffected eomi cognition intact |
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tx of als
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riluzole can delay death by 3-5 months
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tx of trigeminal neuralgia
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tx with carbemazepine
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course of trigeminal neuralgia
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has a relapsing, remitting course
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what does cerebral perfusion pressure (cpp) =
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cpp = mabp - icp
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what relationship is there between jvp and icp
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if jvp is elevated then the csf can't get reabsorbed so icp gets elevated
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what causes vasoconstriction in the barin
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alkalosis
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clinical features of juvenile myoclonic epilepsy
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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 |
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features of frontotemporal dementia
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personality changes, loss of initiative, slowing of thought, preserved recent memory
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clinical features of spinal muscular atrophy
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no sensory abnormalities
--> symmetric proximal muscle weakness and atrophy |
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clinical features of charcot marie tooth dz
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distal muscle atrophy
weakness sensory loss hammer toes |
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pathophys of cervical spondylosis
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chronic d/o of degenerative and hypertrophic changes of vertebral ligaments and disks
--> narrowed spinal cord canal --> compression |
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what anti-epileptic drugs are best tolerated in elderly
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gabapentin
lamotrigine |
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clinical features of vasculitic neuropathy
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acute onset of asymmetric weakness and sensory loss and severe pain
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who gets vasculitic neuropathy
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dm
sle other vasculitides |
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clinical features of paroxysmal hemicrania
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unilateral headache of seconds to minutes in duration
these ha are disabling |
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tx of paroxysmal hemicrania
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indomethacin
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