Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/83

Click to flip

83 Cards in this Set

  • Front
  • Back
major output pathways for the cerebellum
projections to motor cortex (thru the thalamus) and direct connections w/ brainstem motor pathways (rubrospinal, vestibulospinal, reticulospinal)
Cerebellar disruption/dz is a/w what action
precise coordination
hallmark signs of cerebellar disruption
intention tremor, dysdiadochokinesis, limbs ataxia/lack of balance, poor coordination in the absence of weakness
gait of a cerebellar lesion
wide base, swaying/ falling towards the side of dysfunction
cerebellar diseases are more severe when they involve what?
deep nuclei or superior cerebellar peduncle
3 broad areas of cerebellar syndromes=
vestibulocerebellar, spinocerebellar, pontocerebellar
vestibulocerebellar controls
flocculonodular lobe: equilibrium, eye muscles, axial body musculature
Spinocerebellar controls
posture and lower limb mostly, axial body musculature
pontocerebellar
upper limb movement, speech, eye movement
lateral vs medial cerebellar lesions
lateral: more limbs, speech and hearing (AICA); medial: axial musculature, balance, gait, eye movements + brainstem signs (PICA)
hyperkinetic cerebellar syndromes:
essential tremor: inherited. increased thalamic drive. Disorders related to basal ganglia. Affect is symmetrical and freq is constant. tx: propranolo, primidone & surgical manipulations
what inhibits the normal excitatory drive to motor cortex?
globus pallidus
decreased postural tone d/t basal ganglia is because what?
increased excitatory drive to the thalamus which resulted in an increased drive in motor cortex which increases the inhibition of cortex on brainstem tracts --> decreases the postural tone
MC hypokinetic disorder
parkinson's dz
environmental toxin that can cause parkinsons
manganese
differential feature of other hypokinetic disorders vs parkinsons
failure to respond to L-dopa
MC hyperkinetic disorder
Huntington's Chorea
what is destroyed in hemiballismus?
subthalamic nucleis
Definition of Tourette's disorer
hx of both motor & vocal tics > 1 yr onset before 18
what are the 5 examples of hyperkinetic disorders?
Huntington's Chorea, Hemiballismus, tardive-dyskinesia, Athetoid, Tourette's
primary receptors a/w temperature detection
transient receptor potential channels (TRPs)
perception of temperature pathway
DRG--> spinal cord--> brainstem --> thalamus--> insular cortex
pathway for regulation of body temp
ALS --> reticular formation--> hypothalamus
anterior hypothalamus? posterior hypothalamus?
ant: detects temp (heat sensitive)--> preoptic nuclei; post: controls "set point"
caudolateral area of hypothalamus
sympathetic heat conservation
hypothermia temp
95 or <35
physiological responses to hypothermia based on temp
35-32: shivering; 33: clouding of consciousness; 28-32: dec in metabolism; <28: poikilothermia, EEG slowing (<20)
what reflexes stay normal until <82 deg F?
respiratory and tendon reflexes
Heat stroke vs heat exhaustion
stroke: rapid temp increase, CNS sxs; exhaustion: inc over a couple of days, no CNS sxs
DDX: fever & rash involving palms & soles
erythema multiforme, coxsackie A or enterovirus, nisseria, Rickettsia rickettsii, subacute bacterial endocarditis, toxic shock syndrome, VZV, treponema pallidum
FUO-classic
>38.2 on several occasions for at least 3 weeks. + 3 hospital days or 3 outpt visits w/ no dx
FUO-nosocomial
>38.2 on several occasions, for at least 3 weeks, but starts after being admitted to the hospital, uncertain dx after 3 days including 2 day micro culture
FUO- neutropenic
>38.2 on several occasions for at least 3 weeks + neutrophil count <500 + 3 days including 2 day micro culture
FUO- HIV assoc
>38.2 several occasions for 1 months (outpt) or at leats 4 days inpt + confirmed dx of HIV + uncertain dx after 3 days including 2 day micro culture incubation
4 categories of illnesses that account for the maj of FUO
infections (tb MC), malignance, CT dz, misc
SIRS criteria
at least 2 of the following: hyperthermia (>38.5) or hypothermia (<35); tachycardia > 90; tachypnea (>20) or hypocapnia (<32); Leukocytosis (>12,000) or Leukopenia (<4000) or 10% immature bands
Sepsis criteria
SIRS in response to documented infection
severe sepsis
sepsis criteria + 1 of the following: mottled skin, capillary refill >3 secs, urinary output of <.5 ml/kg for at least 1 h, lactate > 2 mmol, abrupt change in mental status or abnormal EEG, thrombocytopenia, DIC, ARDS, cardiac dysfunction
Septic shock
Severe sepsis + 1 of the following: Diastolic BP <60 after fluids or pressors needed to maintain a BP >60
goal of CVP? MAP? Central venous O2 sat?
CVP: btwn 8-12; MAP >65, CVP >70%
who is given RhAPC?
pts w/ sepsis induced organ dysfxn & deemed high risk of death
motor planning originates in?
cerebral cortex
motor coding occurs in?
basal ganglia (learned movement)
motor output is conducted thrus?
motor cortex & corticospinal/ bulbar tracts
supplemental motor cortex controls what?
coordinating between 2 hemispheres
Premotor cortex controls what?
transfer between 2 hemispheres (learned movements)
Transcortical ideomtor apraxia
Caused by anterior cerebral artery--> loss of command to opposite side (can't send the message across the corpus callusum)
what provides inhibition of brainstem pathways that are tonically active?
cortex--> like rubrospinal, vestibulospinal, and reticulospinal tracts
loss of cortical input on brainstem's tonically active tracts causes
disinhibition (Extension)
charcot's triad for MS
nystagmus/intention tremor/scanning speech
very common initial manifestation for MS?
sensory changes: radiculitis/ radiculopathy mostly to trunk or abdomen
lhermitte's phenomenon
electrical shock sensation upon flexion of the neck down spine and into sacrum
gait a/w MS
scissor gait
uhthoff's phenomenon
small increase in body temp increases sxs & sns
dawson's fingers
plaques at centrum semiovale and at right angles to corpus in radiating manner--- MS
tx for acute attacks of MS
GCs (prednisone or methylprednisone)- pulsed
dz modifying tx for MS
interferon B and glatiramer acetate. Everyone with dx should be given INF beta or flatiramer acetat
Glatiramer is a potent inducer of what?
TH2 (sim structure to Myelin basic proteins)
what two dz modifying txs for MS can cause PML? which one can cause cardiotox? ITP?
PML= rituximab, natalizumab; cardio: mitoxantrone; ITP: alemtuzumab
what two myopathic categories causes asymmetric weakness?
neuropathic and infectious
Ribonucleotide protein= marker for what AI dz?
mixed CT dz
myositis specific abs?
jo-1 (anti-tRNA synthetases) syndrome--> inflammatory myopathy w/ ILD, raynaud's, arthritis & mechanics hands
mechanics hands + raynauds + arthritis=
jo-1: myositis
polymyositis and dermatomyositis criteria
PM: 4 out of the 5 = definite, 3 out of 5 = probably; DM: 3 out of 4 + rash= definite, 2 out of 4 + rash= probable. symmetric proximal muscle weakness, incr muscle enzymes, myopathic EMG abnormalities, typical changes on muscle biopsy, typical rash of dermatomyositis
when to hospitalize your myopathic pt?
CK > 10,000 or loss of neck flexors; dysphagia w/ aspiration, profound weakness w/ inability to care for self or walk.
tx for dermatomyositis
hydroxychloroquine
statins + muscle dz
relative contraindication.
UMN 7th lesion=
pt will get weak on lower part of face (contralateral)
LMN 7th lesion=
will affect upper & lower face so they can't close their eye. (ipsilateral)
Stereognosis & extinction are both a/w what section of the brain?
parietal lobe (right)
spastic gait is seen after what 3 circumstances?
after stroke, MS, spinal cord lesion
cushing's triad
HTN, bradycardia, irreg RR
loss of pain & temp on 1 side of face and loss on opposite side of body=
brainstem lesion
loss of pain & temp on 1 side of body and weakness w/ or w/o vibration on opposite side=
spinal cord lesion
pure motor sxs=
C/L small vessel lacunar infarct of the internal capsule, basal ganglia, pons
pure sensory sxs=
C/L small vessel lacunar infarct of the thalamus
psychophysiologic sxs of vertigo
panic attack/anxiety-- numbness & tingling around lips
dix-hall-pike
BPPV dx
photophobia + > 24 hr vertigo
migraine
tx of bell's palsy w/ vesicles on the ear
NOT steroids- acyclovir
MCC if lateral medullar syndrome
PICA--> vomiting, nystagmus, vertigo
sudden HA + acute vertigo + inability to ambulate=
cerebellar hemorrhage
long term tx of MG
Azathioprine & mycophenolate mofetil (purine antagonists)