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PSYCH Flashcards

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1
Q

txt for organophosphate poisoning

A

Atropine - Anticholinergic
tragets the muscarinic receptors

Pralidoxime - reactivates the AcE
targets muscarinic and nicotinic

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2
Q

S1p1 receptor analogue txt for MS

A

Fingolimod, MOA : sphingosine 1 phosphate receptor analogue , interferes with maturation of lymphocytes in lymph nodes

  • inactivates the S1p1, 0.5mg OD
  • WOF bradyarrythmia , macular edema
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3
Q

Monoclonal Ab that can cause PML?

MOA

A

Natalizumab - targets alpha integrin, prevents mono and lymphocytes adhesion to endothelial cell and migration to vessel wall.

SENTINEL study- natalizumab causing PML
Req for Anti-JC virus Ab prior to using Natalizumab for 24 mos and if with hx of prior imuunosupp- risk is 11 in 1,000 pxs.

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4
Q

Charac of PML gross and micros

A

Multifocal subcortical WM lesion with cavitations
No mass effect or edema
Hallmark: Enlargement of oligodendrocytes

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5
Q

Causes of PML

A

Most common - HIV 80%
Immunosuppressive states
lymphoma, CML
nonneoplastic gnaulomatosis (TB, sarcoidosis)
use of dx Natalizumab in 20% , or retroviral rxs
SLE, Pregnancy

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6
Q

Prognosis of PML

A

if untreated - 3-6mos

TXT : anecdotal
cytosine arabinoside, cidofovir, mirtazapine, interferon, and topotecan

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7
Q

A syndrome, in which a fulminant inflammatory response surrounding PML lesions in relation to
rapid treatment of the underlying immunosuppressive
state

A

IRIS (immune reconstitution inflammatory syndrome)

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8
Q

PML occurs in CD 4 count :

A

less than 200, most often less than 50

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9
Q

Dopamine Hypothesis in schiz

A

Schiz is too much dopamine
- antipsychotics/ D2 blockers are effective
_ Dopamine agonist (cocaine and amphetamine ) induces psychomimietic symptoms
- D2 receptors are found in caudate , D4 entorhinal cortex
- loss of GABAergic neurons in hippocampus

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10
Q

Serotonin Hypothesis in schiz

A

serotonin excess as a cause of both positive and negative symptoms in schizophrenia.

serotonin antagonist activity of clozapine

NE may have a role in anhedonia but inconclusive
Ach and Nicotine- dec muscarinic and nicotinic receptors in the caudate-putamen, hippocampus, and selected regions of the prefrontal cortex., cognition

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11
Q

Neuropathology in schiz

A

Enlarged ventricles - 3rd and lateral
Reduced symmetry in temporal, occipital, frontal lobes
Dec in size - amygdala, the hippocampus, and the parahippocampal gyrus.
Dec in size thalamus- Dorsomedial , neurons , oligo, astrocytes reduced by 35-40%
C ell loss or the reduction of volume of the globus pallidus and the substantia nigra. Increase in the number of D2 receptors in the caudate, the putamen, and the nucleus accumbens.

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12
Q

Where is the dysfunction :
positive symptoms
negative
cognition

A

positive - dysfunction of the anterior cingulate basal ganglia thalamocortical circuit
negative - DLPFC
cognition - dec muscarinic and nicotinic receptors in the caudate-putamen, hippocampus, and selected regions of the prefrontal cortex (prefrontal, inferior parietal)

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13
Q

BDNF is dec or inc in depression?

A

Decrease.
stress leads to dec in BDNF, w/c will cause dec in synaptic plasticity then dec in glutamate, dec in synaptic transmission and inc in neuronal degeneration. leading to further depression, cognitive effects as well.

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14
Q

Criteria for Bulimia nervosa

A

A. Binge eating
B. Inappropriate compensatory behaviors to avoid weight gain
C. Self evaluation- body shape and weight
D. 1/wk/ 3 mos

Diff with Anorexia nervosa binge type- ito below BMI pa din

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15
Q

Criteria for PTSD

A

A. Experiencing actual threat/ seriou injury/ sexual violence
B. Intusive thoughts 1/more
C. Avoidance
D. Alterations in cognition or mood
E. Altertaions in arousal and reactivity
F. more than 1 month

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16
Q

Diff of Acute stress disorder from PTSD ?

A

3days -1month symptoms, almost same

share criteria A, and at ASD 9 or more of the ff : intrusion, avoidance, arousal, negative mood and dissociation.

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17
Q

Difference between Bells palsy and Ramsay Hunt syndrome ?

A

Both - peripeheral facial palsy

Bells - HSV , loss of taste, hyperacusis
- inflammation of the geniculate ganglion, int acoustic to the stylomastoid foramen

Ramsay - Varicella zoster , pain, active herpetic lesion
may involve other nerves ( VIII) , nystgamus, tinnitus, hearing loss

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18
Q

Give ex of lesions in the Int acoustic meatus, ganglion and what clinical ?

A

Bells palsy
Gradenigo syndrome

Stylomastoid foramen- mass, SCC, parotid neoplasm
- fibers from facial motor and trigeminal

Chorda tympani- mass lesion
- taste ( nucleus soltarius) and salivation ( sup salivatory nucleus)

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19
Q

If the taste is impaired in px with Bells’s palsy , where is the lesion?

A

lesion is probably proximal to/ at where the chorda tympani joins the facial nerve .

chorda tympani distal to it- taste and salivation

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20
Q

What is most favorable sign in Bells?

A

taste returns in the first week, it is a good prognostic sign. But early recovery of some motor function in the first 5 to 7 days is the most favorable sign.

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21
Q

Gove diff for Bells’s ?

A

Ramsay Hunt
Lyme
HIV
Parotid galnd tumor or invasion of temporal bone

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22
Q

Bilateral facial paralysis ?

A

Developmental - Mobius syndrome
GBS
Heerfordt syndorme- bilateral parotid galnd sweling from sarcoidosis
Melkersson-Rosenthal syndrome- triad of
recurrent facial paralysis, facial (particularly labial) edema, and less constantly, plication of the tongue.
Kennedy’s- with fasciculations as well,

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23
Q

contents of jugular foramen ?

A

9,10,11 nerves
IJVein
sigmoid sinus
meningeal branch from occipital and ascending phary geal arteries

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24
Q

Most common forms of inherited peripheral neuropathy ?

A

CMT

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25
Clinical features by age ?
childhood - clumsiness, foot defromities, high arch and hammertoes , ankle fractures , foot drop Adolescent- inverted champagne bottle
26
Diff betweeb CMT 1 vs CMT 2 ?
CMT 1- first decade of life , enlargement of the nerves in type 1, most easily appreciated by palpation of the greater auricular and peroneal nerves. Dmyelinating, CV is less than 20m/s CMT 2- second decade , CV is around / less than 38m/s
27
other feautres of CMT ?
paresthesias and cramps, hands are involved alter on | NO Autonomic dys
28
Most prevalent CMT ?
CMT 1A 17p, duplication of PMP 22 HNPP - also on ch 17 but is deletion rather than duplication
29
What do CMT 1 and 3 share in common?
Both are dmyelinating, and have onion bulb appearance of schawann cells and fibroblast on microscopy . CMT 3- Dejerine-Sottas disease
30
What is/are the initial neural symptoms of Botulism ?
blurred vision and diplopia are the initial neural symptoms;
31
Differentiate Botulism vs. MG
Both are on NMJ , presynaptic- Botulism like lambert eaton post - MG
32
Differentiate Botulism vs GBS ?
Botulism - Clostridium botulinum , NMJ presynaptic - initial symp are diplopia, blurring of vision, no accommodation/ pupil reflex , severe constipation - CSF normal GBS- peripheral demy, after Campylobacter - has autonomic symptoms, less in sensation ( vibration/position sense) - CSF albuminocytologic dissoc both- less DTRs , weakness
33
TXT for botulism, w/c enhances release of Ach
Guanidine Hydrochloride 50mg/kg Antitoxin 10, 000 U Metronidazole/Penicillin
34
Diff Botulism vs. Tetanus
Botulism- Clos botulinum/ toxin Tetanus - Clost tetani , tetanospasmin - zinc protease blocks NT release - inhibits GABA - affects the Renshaw cell ( source of inhibition of spinal and brainstem neurions ) - masseter most affected = lockjaw - toxin acts directly on skeletal muscle at the point where the axon forms the endplate (accounting perhaps for localized tetanus) and also upon the cerebral cortex and the sympathetic nervous system in the hypothalamus.
35
Most common form of tetanus?
Generalized - Trismus- most freq initial manefestation - risus sardonicus - ophistotonus - tetanic seiz/ convulsions
36
T/F no pathologic changes in muscles, nerves, spinal cord, or brain, even in the most severe generalized forms of tetanus
True Death rate is 50%
37
The most benign form of tetanus ?
Localized tetanus - initial symptoms are stiffness, tightness, and pain in the muscles in the neighborhood of a wound
38
Tetanus that involves head / face ?
Cephalic tetanus- incubation period is 1-2 days
39
EMG of px with tetanus
loss of the physiologic silent period that occurs 50 to 100 ms after reflex contraction.
40
Txt of tetanus ?
Antitoxin (3,000 to 6,000 U of tetanus human immune globulin) should be given along with a 10-day course of penicillin (1.2 million U of procaine penicillin daily), metronidazole (500 mg q6h intravenously or 400 mg rectally), or tetracycline (2 g daily). muscle relation and sedation- benz, baclofen, botox is fails NM blocking agents
41
Immunization for tetanus ?
Anti-toxin Toxoid every 10 yrs as booster if px does not have a booster / toxoid, give one then 2nd dose is after 6 weeks If none at all- give both antitoxin and toxoid
42
Sequence of presentation ICH?
1. Putamen 2. White matter ng temporal, frontal, parietal 3. Thalamus 4. Cerebellum 5. Pons ``` lacunar putamen and caudate Thalamus pons ic hemisphere ```
43
Areas of hypothalamus for hunger and satiety ?
Medial - satiety Lateral - hunger Lateral - Lamon
44
bilateral median SSEP scalp responses are absent in the setting of preserved Erb’s point (N9) and cervical spine (N13) responses
Bad prognosis in post anoxic pxs, done Day 1 post event
45
T/F. Visual acuity affects VEPs only if it is severely impaired (worse than 20/200).
True
46
P100 is expected to be absent where? | cortical vs ocular blindness
Absent in the ocular blindness, P100 represent the waveform from LGN to the calcarine cortex, not generated in the visual cortex. Anton syndrome- P100 is still present VEP- sensitive to lesions of the optic nerve anterior to the optic chiasm
47
occipital cortex is sensitive to flash/ light , T/F
Flase- relatively insensitive. sensitive to edges of contrast= checkboard
48
types of VEP and give indications
Flash VEP- baby, uncooperative pxs, media problems Pattern reversal VEP- most clinically used Pattern onset/ offset - malingering/ nystagmus
49
parameter to look in a px with poor acuity in VEP ?
Acuity= amplitude lesion along the pathway= latency B/L asymmtery= abnormality ( both post chiasmatic area covered in sibgke flash/pattern)
50
VEP in patient witrh NMO/ MS ?
prolonged latency p100 compressive optic nerve lesions- reduced amplitude
51
Degenertaive dse ( huntington's , friedreich ataxia , neurosyphilis, aids/hiv) affect the optic nerve
can alseo cause delay in VEP
52
Px 18-25y/o, initially with aching over eyebrow and eye, ff by sudden blindness, central then peripheral. Dx and results on VEP ?
Leber Hereditary optic Atrophy - pathologic mito DNA hyperemia of disc, peripapillary vasculopathy loss of retinal cell ganglion layer, retinal nerve fiber layer VEP- prolonged latency in P100 change in morphology , later on amplitude also decreases
53
Triad of Retinitis Pigmentosa
retinal pigmentation attenuated vessels/ dec pallor disc
54
Metabolic cases that could cause prolonged latency on VEP;
thyroid opthalmopathy\ | Subacute combined degeneration- also with an SSEP
55
VEP in AION( anterior ischemic optic neuropathy)
Normal latency, low amplitude also in AMbylopia Normal amplitude- 10+/- 4.2 uV
56
VEP in albinism?
Misprojection of optic nerve fibers - Nerve fibers that originate in the temporal retina are misrouted at the optic chiasm. This misrouting results in an anomalous temporal nerve fiber decussation and an abnormal projection to the occipital cortex.-definite VEP asymmetry
57
What to do in px with opaque media for VEP?
use Flash VEP An amplitude reduction of more than 50% or a latency delay of more than 15 ms is highly suggestive of dysfunction in the central visual field.
58
Galucoma in VEP?
prolonged latency and dec amplitude
59
Hemianopic visual pattern vs chiasmatic lesion in VEP ?
hemianopic visualpattern- asymmtery in amplitude recorded over each hemispheres Chiasmatic- reduced amplitude VEP on contralat hemish, when each eye is stimulated separately.
60
Indicate lesions on BAER
wave I- lesion on 8th C.N. - sensorineural and conductive hearing loss - if changes in I and lost of all others- vascular comprise - - if I is unaffected, III and V are affected- injury to the intracranial portion of the auditory nerve waveII - can be absent in NL wave III- good indicator of changes in neural conduction of the auditory nerve. Identification may be difficult in • Absence of wave II • Partial fusion of wave IV and V • Bifid wave III wave IV- shares the same peak with wave V wave V- Most consistent peak of BAEP, • Requires lowest threshold for stimulation ,Highest amplitude of all waveforms= if change kahit na wala change as III- there will still be bloody supply compromise
61
Imp interpeak latency changes in BAER
1. changes in function structures of generators rostral to wave III (cochlear nuclei) - no change on wave III , but WITH change in wave V peak latency and interpeak latency bet III and V . wave I -wave III - CPA - SAME- schwannoma, Aneurysm/ Arachnoid, Meningioma/ mets, Epidermoid/ependymoma wave III- V interpeak- caudal pon sto midbrain, Demyelinating plaques, infarcts, and neoplasms Pathological 4 and 5 wave complex suggestive of basilar artery occlusion distal to AICA.
62
T/ F. 1. absent all waves - brain death in BAER 2. Normal variant in absent III, intact I and V
False Brain death- wave I change/ NL then absent others all absent- severe hearing loss/ large acoustic neuromas Normal BAER- metabolic/toxic enceph
63
Is there a hearing loss in absent I , intact III and V ?
Yes. peripheral hearing loss
64
Effects in BAER of temp and BP
Temp- every C drop= 0.2ms inc in latency of wave V BP- drop in BP- dec amplitude and inc latency of wave V Age - older have inc interpeak latency Gender- female shorter latency anes and NMB agents- no sig effects
65
When should newborn hearing screening must be done?
3-5 month of age, 30db
66
Factors that influence the NCS
Temp-every C drop in temp, fastest motor NCV is reduced by 1m/s limb length / height Age- sensory conduction halves with age
67
Some idiopathic cause of trigeminal neuralgia are found out to have:
idiopathic cases are caused by compression of the trigeminal roots by a small tortuous branch of the basilar artery. Txt: decompression Pharma Carbamazepine is effective in 70 to 80 percent of patients (600 to 1,200mg/day ) phenytoin (300 to 400 mg/d), valproic acid (800 to 1,200 mg/d), clonazepam (2 to 6 mg/d), gabapentin (300 to 900 mg/d or more), pregabalin (150 to 300 mg/d),
68
paroxysm of pain usually over the V2-V3, which is followed by a refractory period of up to 2 or 3 min, no sensory or motor deficit, response well to AED stimulation of certain areas of the face, lips, or gums, as in shaving or brushing the teeth, or by movement
trigeminal neuralgia Ramsay hunt- more of V1
69
The mean age of onset Trigeminal neuralgia is 52 to 58 years for the idiopathic form and 30 to 35 years for the symptomatic forms, the latter being caused by
trauma or vascular, (basilar) neoplastic (meningioma/ schawannoma, choleastomas, chordomas ) , and demyelinative diseases. WOF “numb chin” sign- affected V3 among metastaic CA
70
What is tic convulsif? and caused by?
trigeminal neuralgia and hemifacial spasm cause: tumor (cholesteatoma), an aneurysmal dilatation of the basilar artery or one of its branches, or an arteriovenous malformation
71
Most commonly associated with inflamm and infectious cause of trigeminal involvement ?
Herpes zoster
72
Triad : Facial pain, otitis media/ osteomyelitis of petrous bone, abducens nerve involvement
Gradenigo syndrome Tolosa Hunt- Facial pain, opthalmoplegia, inflamm of sof / cavernous sinus
73
Possible toxic cause of trigeminal neuropathy
toxicity from stilbamidine and trichloroethylene is known to cause sensory loss, tingling, burning, and itching exclusively in the trigeminal sensory territory
74
Rapid or subacute dementia Myocolnic jerks Prodrome- fatigue, depresaion like, ataxia visual distortions
CJD Patho: widespread neuronal loss Jerks- 2nd to loss of inhibitor cells in the thalamic reticulum
75
Dx of CJD
Csf is normal Imaging- cortical ribbon sign ( occipital) similar to cerebral anoxia Hyperintense in T2 basal ganglia Immunoassay 14-3-3 Eeg- nonsp slowing or high voltafe slow 1-2Hz Txt- no specific only sensitive to autoclave/ immersion to bleach 5% in 1 hr
76
Good diff for CJD
Myoclonus + Dementia= whipple, intravas lymphoma,carcinomatous menigitis Or alz-CBD
77
Gertsmann SSS is another prion dse caharacterize
Moatky cerebellar symptoms - nystagmus, dysarhtrua, ataxia, CSR - normal MRI but has spongiform changes in brain like CJD
78
Prion diasese with mutation in codon 178
Fatal insomnia - dementia, intractable insomnia , symp overactivity Neuronal loss- medial thalamaic nuclei vs. CjD ( gen neuronal loss)
79
Laughing sickness, death wiyhin 3-6mos
Kuru Progress ataxia, ocular abn movts Spongiform changes in brain esp cerebellum Astroglial prolif stellate amyloid cells- Kuru plaques
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