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261 Cards in this Set
- Front
- Back
What are the main features of isolated syndrome of the first presentation of MS?
|
Optic neuritis
Transverse myelitis Brainstem syndrome |
|
What is the clinical presentation of transverse myelitis?
|
Disthesia
Paraplegia |
|
How does brainstem syndrome present?
|
Double vision
Lack of balance Incoordination |
|
Name three variant forms of MS
|
Marburg's variant - severe axonal loss
Balo's concentric Sclerosis Neuromyelitis optica |
|
How can diffuse lesions seen on MRI be diagnosed as MS
|
Temporal dispersion
Spatial dispersion of demyelinating disease activity. |
|
ADEM
|
Acute Disseminated Encephalomyelytis
|
|
Onset of ADEM
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2-3 weeks after a viral infection
|
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ADEM is monophasic:
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Happens once, after the insult and has an endpoint. all the lesions are of the same age.
|
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Dawson's finger:
|
Seen with multiple Sclerosis, a plaque which is perpendicular to the lateral ventricle.
|
|
True or False:
MS is both a demyelinating disease and one that causes axonal injury. |
True
|
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What does multiple in MS mean
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Lesions are multiple in space and happen at different (multiple) time.
|
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Symptoms of X-linked adrenoleukodystrophy in children (age 4-8)
|
ADHD like
Progressive impaired cognition Behavior, Loss in vision and hearing *** loss of milestones *** |
|
Symptoms of X-linked adults:
|
More like primary progessive MS
|
|
How do you diagnose X-ALD?
|
Mostly males (x -linked)
MRI - abnormal Increased VLFCA - Very Long Fatty Chain Acids |
|
Symptoms of subacute combined degeneration in B12 deficiency
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Weakness
Abnormal sensation Mental problems Vision difficulties |
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What nn does peripheral neuropathy involve?
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Sensory
Motor Both |
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How does peripheral neuropathy present, sign:
|
Reduced or absent muscle reflexes.
Distal - proximal weakness Atrophy Reduced sensation |
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List Five peripheral neuropathy patterns:
|
Distal symmetric neuropathy
Mononeuropathy Multiple mononeuropathy Autonomic neuropathies Small Fiber neuropathy |
|
Distal symmetric neuropathy -
Etiologies |
Diabetes and toxic neuropathies (chemo and toxic alchohol use)
|
|
Mononeuropathy - Etiologies
|
One nn affected
Carpal tunnel syndrome (Median NN pinched - weak hand) Ulnar neuropathy - numb and tingling of medial 2 fingers Perineal neuropathy @ fibular head (Foot drop) |
|
Multiple mononeuropathy
(Assymetric, more than one nn, possible nn infarction) |
Inflammation with autoimmune disease eg. LUPUS, Polyateritis nodosa
|
|
Clinical Features Autonomic neuropathies:
|
Dysautonomia eg. urinary retention, erectile dysfunction, postural HTN.
|
|
Autonomic neuropathies:
***ETIOLOGIES *** |
Diabetes
***AMYLOIDOSIS *** |
|
Small Fiber neuropathy: Symptoms
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Tingling/ Burning/ Pain sensation.
|
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Small Fiber neuropathy: Signs
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Abnormal neurological exam but EMG/NCS normal (examine large fibers)
|
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Small Fiber neuropathy: Dx
|
Count small nn fibers (less) on epidermal nerve fiber assessment by skin biopsy.
|
|
What is Charcot-Marie Tooth (CMT) disease:
|
Most common inherited neurological disorder
Can be AD (More), AR, X-linked. Affects peripheral myelin - uniform demyelination |
|
What are the patterns of peripheral nn damage?
|
Neuronal damage (ALS, Sjorgen's disease, Anti-HU paraneoplastic disease)
Axonal inury (Wallerian degen and atropy of muscles) Demyelinating disease (Guillain-Barre & CIDP) |
|
What is Guillian-Barre syndrome?
|
Aquired autoimmune disorder
Recent URI or recent vaccine First tingling and weakenss of legs --> weak arms May not be able to breath with time. Arreflexia. Usually transient, could revert to normal in a few weeks. Normal sensory function. |
|
What tests would you do if suspect Guillan-Barre syndrome.
*** MUI IMPORTANTE *** |
EMG MAY BE NORMAL IMMEDIATELY AFTER ONSET, DON'T DO THIS.EMG WOULD BE NORMAL EARLY.
TAP CSF - CHECK FOR INCR. PROTEIN CONTENT WITH NORMAL CELLULARITY. |
|
Rx of Guillain Barre syndrome:
|
DO NOT GIVE STEROIDS - May deteriorate
Give IV Immunoglobulins Plasma exchange - get rid of the antibodies attacking the patients nerves. |
|
What is CIDP (Chronic Inflammatory Demyelinating Polyradiculoneuropathy)?
|
Chronic variety of Guillain -Barre
Repeated attacks of demyelination slower onset > 8 wks Elevated CSF protein EMG - may see acquired demyelination - conduction block. |
|
Two markers for acquired demyelination
|
Conduction block
Temporal dispersion |
|
Rx of CIDP syndrome:
|
Steroids
IV Immunoglobulins Plasma exchange |
|
What is Parsonage-Turner Syndrome (Aka Brachial plexus neuritis)?
Signs and symptoms |
Preceeding hx of vaccination, infection, diabetes, Sjorgens
Burning pain in arm Weakness numbness Atrophy of nerve may dvp. Weakness of muscles innervated by anterior interosseous (branch of median nn) Weak flexor pollicus longus & Flexor digitorum profundus |
|
Name three motor neuron diseases:
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ALS
Spinal Muscular atrophy Spinal Bulbar Muscular atrophy (kennedy disease) |
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Which motor neuron disease is X-linked, have CAG repeats with anticipation?
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Spinal Bulbar Muscular atrophy (kennedy disease)
|
|
Which motor neuron disease is Autosomal recessive and has mutation in ***chromosome 5Q ***?
*** MUI IMPORTANTE *** |
Spinal Muscular Atrophy (Presents as floppy infant"
|
|
What is common about the sensory system in motor neuron diseases?
|
Have normal sensory
|
|
(3) NMJ disorders
|
Myasthenia Gravis
Eaton-Lambert Syndrome Congenital myasthenia |
|
Are there sensory symptoms associated with NMJ?
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NO, NMJ between motor nn and muscle.
|
|
What is Myasthenia Gravis?
|
Acquired
Autoimmune Weakness (Ocular - eyelid ptosis [ Binocular diplopia ...symptoms flactuate], limb weakness and bulbar fatigue [trouble swallowing, chewing, breathing] |
|
What is the pathology of Myasthenia Gravis?
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Antibodies againts Ach or Muscle Specific Kinase (MuSK - against tyrosine kinase), simplifaction of postsynaptic membrane.
|
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What are the symptoms of Ocular MG?
|
Eyelid ptosis/ diplopia without generalized weakness.
|
|
Diagnosis of Myasthenia Gravis?
|
Flactuating weakness pattern, usually more proximal.
Check receptor ab. NCS - repetitive nn stimulation and observe ampl of signal. Decr. response suggests affect postsynaptic end. Tensillon test Ice pack test - cooling eye may resolve ptosis, help eye muscle depolarize synchronously. |
|
Describe Tensillon test that is used to diagnose MG.
|
Tensillon test - Achesterase inh, inh break down of Ach, prolonging Ach, help patient sustain muscle contraction.
|
|
What tumors are associated with MG?
|
Thymic tumors (10-15%), diagnose by CAT scan. Removing tumor can improve response of disease to treatment.
|
|
How is MG treated?
|
AChesterase inhibitor - treat symptoms
Immunosuppresant drugs: Steroids, steroid sparing agents, IVIg, plasma exchange |
|
What is the difference between neonatal MG and congenital MG disorders?
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The latter last longer than 12 weeks and are due to defect in NMJ. The neonatal MG is due to antibodies present due to having a mother that has MG. Usually lasts 12 wekks.
|
|
Vast majority of Congenital myasthenia gravis disorders are inherited in an:
*** MUI IMPORTANTE *** |
AUTOSOMAL RECESSIVE FASHION
|
|
What is the majot difference between the pathology of Lambert Eaton myasthenic syndrome (LEMS) and MG?
|
LEMS - acquired autoimmune disease that affects the presynaptic terminal.
MG - acquired autoimmune disease that affects the postsynaptic terminal. |
|
What diseases are associated with LEMS?
|
Small cell lung cancer
Lymphomas |
|
Why do LEMS improve with exercise or electrical stimulation in lab?
|
Antibodies to presynaptic membranes and interferes with the release of Ach vessicles. As use muscle more, allow more Ach to be released and thus available and hence less symptoms.
|
|
Why do we see upregulation of postsynaptic folds with LEMS?
|
Lack of enough Ach leads to upregulation of receptors on postsynaptic memrbane.
|
|
What is the difference between response of MG to exercise and response of LEMS to exercise?
*** MUI IMPORTANTE *** |
Incremental response with LEMS and decremental response with MG.
|
|
Pathology - what membrane is involved in botulism?
|
Pre-synaptic mebrane - C. botulinum (neurotoxin).
|
|
Symptoms and signs of botulism?
|
Weakness
EOM involved Pupils spared Constipation |
|
What are myopathies?
|
Disorder that affects muscle
Affects proximal more than distal. spillage of muscle enzymes - Aldolase, lactate dehydrogenase, CPK Inherited or acquired. |
|
Signs and symtpoms of myopathies:
|
Weak
Muscle cramps Exercise induced pain Myoglobinuria - due to break down of muscles No sensory symptoms |
|
Inherited myopathies
|
Muscular dystrophy
Metabolic myopathies Congenital myopathies - present with floppy baby syndrome Mitochondrial myopathies |
|
Acquired myopathies
|
Inflammatory myopathies
Infectious myopathies Toxic myopathies |
|
Diagnostic tests for myopathies:
|
Needle EMG
Char small motor unit potentials - short duration and short amplitude Early recruitment - due to weak muscles. NERVE CONDUCTION IS NORMAL Elevations in muscle enzymes and may have elevations of liver enzymes: CK, Lactate, aldolase, AST, ALT Muscle biopsies |
|
Differential Dx of muscle myopathies:
|
Muscle myopathy
Muscle trauma Exercise Increase muscle mass Variation due to ethinicity & gender |
|
What are muscular dystrophies?
|
Hereditary
Progressive with time Degenerative Variable onset in intensity of disease. |
|
Give examples of muscular dystrophies:
|
Duchenne (X-linked, dystrophin)
Becker (X-linked, dystrophin) Limb-girdle (AD, AR, X-linked - affect more hip) Emery-Dreifuss (Contracture of arm muscles, lots of cardiac disease) Facioscapulohumeral Myotonic dystrophy (Difficulty relaxing muscles) Oculopharyngeal muscular dystrophy (mitochondrial diseases) |
|
Give examples of inflammatory myopathies:
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EMG - see denervation
Polymyositis Dermatomyositis - also rashes on skin usually elbows Inclusion body myositis - affects older patients. No response to treatment |
|
Which two inflammatory myosities present in two peaks?
|
Polymyositis
Dermatomyositis - 2nd peak usually associated with cancer. |
|
How would you evaluate a possible toxic myopathy caused by Lipid lowering agents?
*** MUI IMPORTANTE *** |
Check CK levels, DO NOT CHECK EMG, WOULD BE NORMAL.
|
|
Past medical Hx associated with mitochondrial myopathy:
|
Diabetes mellitus
Short stature Sz Deafness |
|
Three syndromes associated with mitochondrial myopathies:
*** MUI IMPORTANTE *** |
Myoclonic Epilepsy with Ragged Red Fibers (MERRF)
Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke (MELAS) Mitochondrial, Neurogastrointestinal Encephalopathy Syndrome (MNGIE) |
|
MRI of Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke (MELAS)?
*** MUI IMPORTANTE *** |
Look like they have stroke but resolves in days.
|
|
What are periodic paralysis?
*** MUI IMPORTANTE *** |
Muscle channelopathies
Occur in episodic attacks Cause transient weakness |
|
Etiology of periodic paralysis?
*** MUI IMPORTANTE *** |
**LARGE CARBOHYRDATE MEALS **
Rigorous exrecise Emotional stress Change in serum potassium levels |
|
Two flavours of periodic paralysis:
|
Hyperkalemic - Ca+ channelopathy, hrs - days
Hypokalemic - Na+ channelopathy, min - hrs |
|
How would you treat hyperkalemic periodic paralysis?
*** MUI IMPORTANTE *** |
ACETAZOLOMIDE
|
|
TRUE OR FALSE
Romenberg is a test of cerebellar function |
False:
Romenberg tests proprioception. |
|
What are Lewy bodies?
*** MUI IMPORTANTE *** |
Cytoplasmic inclusions of alpha-synuclein, seen in Parkinsons Disease.
|
|
What is the difference between Levodopa and Dopamine?
|
Levodopa can cross the BBB whereas Dopamine cannot.
|
|
Complications of Levodopa therapy?
|
Wild movements
Dyskinesia Hallucinations Nausea Orthostatic hypotension |
|
Name some causes of secondary parkinsons:
|
Neuroleptics
Reglan & Metaclopromide - meds. for GI probs. Cerebrovascular stroke MPTP Dementia Pugilistica - Muhammad Ali |
|
The four cardinal clinical features of Parkinsons:
*** MUI IMPORTANTE *** |
Bradykinesia
Resting tremor Cogwheel rigidity Postural instability |
|
First line treatment of PD:
*** MUI IMPORTANTE *** |
Carbidopa/Levodopa
|
|
List 4 Parkinsons plus syndromes:
*** MUI IMPORTANTE *** |
Progressive Supranuclear palsy (PSP)
Dementia with Lewy Bodies (DLB) Multiple System Atrophy(MSA) Corticobasal Degeneration (CBD) |
|
Progressive Supranuclear Palsy (PSP)
*** MUI IMPORTANTE *** |
Gaze palsy, **Fall early on, Nucchal rigidity, Speech disorder.
|
|
What % of strokes are due to Ischemia?
|
80%
|
|
Define lacunar stroke
|
Lake - very small stroke from basilar artery branch occlusion.
|
|
Stroke warning signs:
|
Sudden weakness of face, arm, leg on one side of body
Sudden confusion, trouble speaking Sudden trouble walking, dizzy, lack of balance or co-ordination Severe headaches - Thunderslap- with no known cause |
|
Define TIA
|
Temporary focal neurological deficit of brain related to ischemia or brain or retina < 24hrs. Symptoms clear up after 1hr.
|
|
What part of the brain is improtant for understanding language?
|
Wernickes area
|
|
What part of the brain is speech area?
|
Broca's area
|
|
What artery is involved in patient with: Right hemiparesis, Right sensory loss, Right homonymous hemianopia, Aphasia - (global, Broca's, Wernicke's),Dysarthria (sound drunk), Alexia, Acalculia.
|
Left Middle Cerebral Artery
|
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Define Broca's Aphasia
|
Can comprehend language but their speech is broken.
|
|
Define Wernicke's Aphasia
|
Fluent speech but difficulty in understanding.
|
|
Define Alexia
|
Inability to read words/ text
|
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What symptoms might differentiate a stroke on the right side from left side?
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Neglect of left side, Anosognosia (don't recognise what's wrong with them), Loss of prosody of speech, Flat affect, Extinction, Apraxia
|
|
Define Extinction as a sign for R. MCA stroke.
|
Touch both hands of patient with Right MCA stroke, can only feel touch on the right side
|
|
Define apraxia as a sign for R. MCA stroke.
|
Patients does not know to something which they formerly knew but now they don't.
Dressing apraxia Constructional apraxia |
|
Define Topographic memory deficit as a sign for R. MCA stroke
|
Lost in farmiliar sorroundings
|
|
What are the three main clinical features of Posterior Cerebral Artery occlusion:
|
R/L homonymous hemianopia (contralateral of deficit)
Hemi-ataxia Color-anomia : unable to id colors Prospognosia - if involves parietal lobe- can't recognize faces. |
|
A patient comes in presenting with: Decr. consciousness, contralateral hemiparesis, dysarthria, hoarseness, vertigo, nausea, vomit, hearing loss:
|
Brainstem stroke
|
|
4 nonmodifiable risk factors for stroke:
|
Family history
Age Race Sex - Males more than females |
|
Modifiable risk factors for stroke
|
Htn
Diabetes Cigarrete smoking Hyperlipidemia Obesity Cardiovascular problems ATRIAL FIBRILLATION Alchohol History of previous stroke Carotid stenosis |
|
How do you diagnose a patient you suspect to have a stroke?
*** MUI IMPORTANTE *** |
CT scan - to determine if BLOOD IS INVOLVED (ischemic or hemorrhagic?)
MRI -If CT scan not clear, get more information Echocardiogram - function of heart Arteriography - vessel function |
|
list three etiology classes that are involved in ischemic stroke:
|
Cardiac manifestations
Large vessel disease Small vessel disease Hematological disorder |
|
How do you treat stroke acutely?
|
If stroke is within 3hrs, tPA can be given; Don't give to those with TIA or likely to hemorrahge.
Aspirin - If given within 48hrs of time of onset. Give this if can't get tPA |
|
How are stroke patients surgically managed?
|
Carotid endarterectomy: Do to prevent stroke, if really narrowed artery.
Hemicraneotomy: Stroke patients with swollen brain to decrease mass effect and herniation. |
|
Preventive medications for stroke:
|
Antiplatelet agents (Aspirin, Clopidogrel,Anticoagulation - warfarin/coumadin)
|
|
Define Sz
|
Sudden rythmic change in electrical activity usually accompanied by change in behavior
|
|
Difference betw. simple partial and Complex partial Sz.
|
Both have auras, but complex partial has loss in awareness whereas simple partial does not.
|
|
Who is an epileptic?
|
Had 2 or more unprovoked Sz
|
|
EEG abnormalities in an epileptic:
|
Spikes and sharp waves
|
|
What is the most common cause of medically refractory symptomatic epilepsy:
|
Hippocampal sclerosis - CA1, CA3, CA4 damaged, CA2 spared.
|
|
What is the most common cause of medically generalized symptomatic epilepsy:
|
Global anoxia and tuberous sclerosis
|
|
Name the epilepsy syndrome:
Onset: 4-8yrs old EEG: 3Hz spike and wave Rare GTC Respond well to meds |
Childhood absence Sz
|
|
Name the epilepsy syndrome:
Onset: 12-18 old EEG: 4-4.5Hz spike and wave GTC possible Sz in morning Respond well to meds |
Juvenile Mycolonic Epilepsy
|
|
Name the epilepsy syndrome:
EEG: Charecharestic Multiple Sz types Mental Retardation Not treatable |
Lennox-Gastaut syndrome
|
|
Name the epilepsy syndrome:
Onset: 5-9yrs old Sz: focal motor - unilateral facial twitching. GTC - only at night Normal MRI Only idiopathic partial epilepsy No treatment necessary |
Benign Rolandic
|
|
Name the epilepsy syndrome:
Onset: childhood or adolescence Hx: predisposing hit - complex febrile Sz Origin: Hippocampus / amygdala few GTC Not medically controlled EEG: Focal temporal spikes Aura Automatisms |
Mesial Temporal Lobe epilepsy
|
|
Name the epilepsy syndrome:
SZ - at night mostly Bizarre and complex automatisms Fencers posture May spread to temporal lobe - MTLE |
Frontal Lobe Epilepsy
|
|
Name the epilepsy syndrome:Presents simply with GTC
|
Neocortical epilepsy
|
|
This Sz last for a min like clockwork:
|
GTC
|
|
The Sz that lasts the longest: 2 min
|
Focal
|
|
List 4 types of generalaized Sz
|
GTC
Myoclonic Absence (typical and atypical) Atonic |
|
List 2 types of Focal SZ
|
Simple partial
Complex partial |
|
Name two drugs that can provoke Sz
|
Clozapine and cyclosporine
|
|
Which epipleptic syndrome doesn't need treatment
|
BRE
|
|
Most common aura associated with MTLE
|
Rising epigastric sensation
|
|
Difference between patients energy level after frontal lobe sz as compared to temporal lobe sz
|
Frontal - feel fine
Temporal - tired |
|
Which epipleptic syndrome respond to treatment?
|
CAE
JME |
|
Which epipleptic syndrome do not respond to treatment?
|
Lennox Gastaut syndrome
MTLE |
|
What is the treatment of choice for MTLE?
|
Surgery
|
|
What is the new std of care of Glioblastoma multiforme?
|
Temozolamide with radiation therapy
|
|
4 main cancers associated with brain metastases
|
Lung
Breast Melanoma Colon |
|
Symptoms that a patient with brain metastases may present with:
|
Headache
Seizures - 10% Cranial palsies Focal weakness |
|
When would you resect a single brain metastasic lesion?
|
If patient has KPS>70 and is funtionally independent.
If patient has KPS<70, do it for palliation. |
|
What does this patient have?
Unilateral headache Moderate Pulsating Photophobia and phonophobia Has has this before, no other disorder |
Migraine without aura
|
|
What does this patient have?
Bilateral pain Mild- moderate No aggravated by physical activity No other symptoms excpet slight nausea Non-pulsating No other organic disease 5 previous attacks Each attack lasts 30min to 7 days |
Tension-type headache
|
|
Patient has severe headache in V2 V3 area of trigeminal nn distribution on the face.
|
Trigeminal neuralgia
|
|
What does this patient have?
Severe unilateral pai lasting 15 min to 180 min. Ipsilateral nasal congestion. Has headache every other day Had 6 attacks SMOKER |
Cluster headache
|
|
What are the red flags that might indicate an important secondary headache?
*** MUI IMPORTANTE *** |
Systemic symtoms
Secondary Risk factors Neurologic symptoms Onset: sudden, split second Older Previous headache |
|
A patient with chronic migraine complicated by overuse of medication has:
|
Rebound headaches
|
|
What kind of headache?
Migraine preceeded by one neurological aura |
Migraine with Aura
|
|
Also know as a suicide headache:
|
Chronic cluster headache
|
|
What are the most common neurodegenerative diseases that cause dementia?
|
Alzheimers - 70-80%
Lewy body disease - 10-15% Frontal Temporal Degeneration - 5-10% |
|
Define dementia
|
Progressive disturbance in cognition and can be diagnosed by history and exam - clinically
|
|
Difference between delirium and dementia
|
Delirium: Loss of attention and hallucination over a period of days and usually due to metabolic insult. Reversible.
Dementia: Focal Loss in cognitive abilities over a period of years. Usually have brain lesion and is not reversible. |
|
What is the basic pathway in pathogenesis of neurodegen. diseases?
|
Failed biochem pathway --> accumulation of junk --> neuronal dysfunction and death.
|
|
What are the different parts of papz circuit
|
Hippocampus--> Fornix --> mammilary bodies --> Anterior thalamus --> Cingulate
|
|
When is an EEG used in diagnosing Brain pathology?
|
When suspect epileptic Sz.
Altered levels of consciousness or coma |
|
What is Epileptiform activity seen on EEG?
|
Abnormal brain activity which predisposes a patient for epilepsy. This activity is like a short circuit, presents as a sharp wave.
|
|
You are looking for epilepsy and obtain a normal EEG. What are your conclusions:
|
Cannot rule out epilepsy, may not have picked up activity
|
|
Nerve conduction studies can be done to asses for:
|
Peripheral neuropathy
Charcot-Marie tooth disease Acute demyelinating neuropathy |
|
EMG studies can be done to asses for:
|
ALY
Polymyositis Muscular dystrophy |
|
What are you testing when carrying out evoked potentials?
|
Connection btw peripheral nn and CNS. Combines NCS and EEG. Used in Multiple sclerosis, myelopathy and conversion disorder.
|
|
Describe a digital subtraction angiography
|
Catheter --> femoral artery -->brain artery --> inject contrast --> look for abnormality --> treat with endovascular therapy
|
|
When are CAT scans a preferable technique when assesing the brain?
|
Acute and subacute hemorrhages - bright on scan
Emergencies - takes abt 10 min. Spinal cord imaging - bony images CAT angiography - like X-ray only this is via veins and can be used for non-interventional procedures. |
|
How would you treat a post Lumbar punture headache?
|
Bedrest, fluids, caffeine
If that fails, may need a blood patch |
|
When are MRI's a preferable technique when assesing the brain?
|
Able to discern the structure of the brain.
Allows Dx of: small Strokes (diffusional MRI) MS |
|
Define the term: Delusion
|
A false and fixed idiosyncratic belief
|
|
Define the term: Illusion
|
Misperception of real external stimuli
|
|
Define the term: Hallucination
|
Sensory perception that has compelling sense of a true perception but occurs without external stimuli.
|
|
Describe the pentaxial system that pyschiatrists use in assesing a patient:
|
Axis I - Clinical psychiatric disordres
AxisII - Personality disorders and mental retardation AxisIII - non-pyschiatric disorders Axis IV - Acting stressors Axis V - Global assesment of funtion. |
|
What are the diagnostic criteria of a panic disorder without agoraphobia
|
Recurrent unexpected panic attacks and followed by atleast one month of:
- Fear of attack - - Change of behavior related to attacks - -worry abt consequences of attack- Absence of agoraphobia No other medical or mental disorder 18 -35 yrs old |
|
When do we see onset of panick attacks?
|
18 - 35yrs old
|
|
How do you work up what looks like a panic attack?
|
Hx - medical and pysch
PE and NE Mental status exam Medication hx Drugs? EKG if >40 CBC Thyroid function test |
|
What are the diagnostic criteria of a panic attack
|
Intense fear with four or more symptoms associated with increase adrenaline (abrupt and peak in 10min.)
palpitations sweat trembling Fear of dying |
|
Agoraphobia
|
Fear of being in places where help might not be available. 2.5 - 6% prevalence
|
|
How would you treat panic disorder?
|
SSRI - First line, *lower *concentration than used for depression (Paroxetine, Sertraline, Escitalopram)
TCA's - (Imipramine, Cloripramine) BZD - (Clonazepam) MAOI's - (Phenelzine) Cognitive behavioral therapy - desensitization and behavioral training |
|
How would you treat social phobia?
|
B-Blockers
Generalized phobia - SSRI's and MAOI's |
|
What makes a panic attack a panic disorder?
|
Recurrent unpexpected panic disorder
|
|
Name the different anxiety disorders:
|
Panic disorder
Social phobia Specific phobia OCD Post Traumatic Stress Disorder Acute Stress Disorder Generalized Anxiety disorder Anxiety disorder due to a general medical condition Substance-induced anxiety disorder. |
|
How would you treat OCD?
|
SSRI's - Dose higher than that used to treat depression.
Paroxetine Fluoxetine Sertraline Fluvoxamine TCA - Clomipramine Behavior therapy BZD's - not very useful in treating OCD |
|
What disorder doe this individual have:
He has had this symptoms for >1 month: BOTH: Has experienced lifethreatening event AND This involved intense fear Re-experience thru dreams/ flashbacks Avoidance of stimuli associated with trauma Increased arousal - INSOMNIA, ANGER ... |
Post Traumatic Stress Disorder
|
|
How would you treat PTSD?
|
First line: SSRI - Sertraline
Mood stabilizer - Buspirone *2nd line* Beta-blocker - propanolol Atypical antipsychotics |
|
How would you treat Generalized Anxiety Disorder?
|
First line:SSRI - Venlafaxine
Buspirone - also first line BZD - not very useful Congitive behavioral therapy |
|
Diagnostic criteria for GAD
|
For more than **6 months** patient:
Worries too much Can't control their anxiety Has at least three of the following -Restless -Tired easily -Dificulty concentrating -Irritable -Muscle tension -Sleep distubance DOES ANTICIPATE A PANIC ATTACK Is causing them sig. distress Not using drugs or with any other medical condition |
|
What is the lifetime prevalence of PTSD?
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10%
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In patients with GAD, does their worry tend to serve a defensive function?
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Yes, worry about superficial things so that one doesn't have to deal with the true concern.
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The cell bodies are confined primarily to the locus ceruleus, name the NT
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NE
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Benzodiazepines enhance effects at its receptors;name the NT
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GABA
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The cell bodies are localized primarily within the raphe nuclei;name the NT
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Serotonin
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What disorder is associated with Isolation, undoing, and reaction formation
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OCD
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List (5) mood disorders:
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Depressive disorders
Bipolar disorders Adjustment disorder with depressive mood Aubstance-induced mood disorder Modo disorder due to medical condition |
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What mood disorder does this individual have?
@least 2 wks of persistent mood, cognitive & behavioral symptoms >5 of the following symptoms nearly all the day, nearly all the time **Low mood **Anhedonia- decr. interest in activities **Weight loss/ gain **insomnia/hypersomnia ** Pyschomotor agitation or retardation **Fatigue or low energy **Feel worthless or guilty **Indecisive, impared decisions or memory **recurr. thots of death or suicide |
Major Depressive disorder
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List (3) depressive disorders:
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Major depressive disorder
Dysthymia Depressive disorder NOS |
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Patient presents with Chronic depression, has had it for more than 2 years. The patient has not been without symptoms for more than 2 months during the 2 yrs. Milder than major depressive disorder.
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Dysthymia
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What mood disorder does this individual have?
@least 1 wk *persistent* elevated, expansive or irritable >3 of 7 all in same week: Grandiosity Decreased NEED for Sleep Pressured speech Racing thoughts Distractability Pyschomotor agitation or excessive activity Excessive indulgence in pleasurable with poor judgement. |
Manic episode
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What is this person suffering from:
Mild form of mani <4 days NO PYSCHOSIS No major impairement of function |
Hypomanic episode
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This mood state is a poor prognosis of bipolar, patient has mania and depression at same time and terrible "bouts" of pyschosis
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Mixed episode
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Describe a Bipolar II disorder
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One or more hypomanic episode
and Depressive episode HAS NEVER HAD AN EPISODE OF MANIA |
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Describe a cyclothymic disorder
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Chronic depression (milder than major)
Alternating with hypomania for 2 years, Patient should not be without symptoms for more than 2 months during the 2 yr period |
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Give examples of substances that can induce mood disorder
*** MUI IMPORTANTE *** |
Steroids - Mania
Oral contraceptives - depression Cocaine - induced mania |
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Epidemeology of Bipolar I disorder:
What is the point prevalence? |
1-2%
Males:Females |
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Epidemeology of Bipolar II disorder:
What is the point prevalence? |
0.5%
More common in females |
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Epidemeology of Major depressive disorder:
What is the point prevalence? |
5-9% Female
2-4% male No sex diff in childhood Lifetime prevalence: 20-25% F 7-12%M |
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Epidemeology of Dysthymic:
What is the lifetime prevalence? |
6%
3F:1M |
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Which of the two has the greatest degree of genetic predisposition?
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Bipolar disorder
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What functions of the body are affected by the monoamines involved in Bipolar disorder and major depressive disorder?
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Arousal, Sleep patterns, motivation, aggression, pain perception, basic autonomic regulation and rhythms.
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monoamines involved in Bipolar disorder and major depressive disorder?
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5HT, NE, DA
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What role does NE play in CNS
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Sleep, Arousal, Anxiety, Pain, Activation
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What role does 5HT (5Hydroxytryptamine) play in CNS
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** Most broadly distributed NT in the brain **
Mood regulation, Sleep, pain, agression, memory, appetite, blood pressure, respiratory and pulse rates ** 5HT in CNS decreases depression and axiety at many sites. MAY ALSO PROVOKE AGITATION, SOCIAL DYSFUNCTION AND HEADACHE |
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What role does DA play in CNS
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Pleasure and motivation, structure cognition and emotion, regulate reward in nucleus acumbens and median forebrain bundles
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What is the "finger print of depression" with regards to sleep abnormalities?
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Have decreased REM latency, REM earluer and also altered periodicity. Happens in 45 - 90 minutes in normal people but earlier in those with depression.
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The kindling model of mood disordrs is an endogenous process in the __________ system and might explain why these depressive episodes occur and why we can use Anti epileptic drugs for mood disorders
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Limbic system
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How are patients with excessive activation of hypothalamic-pituitary -adrenal axis likely to respond to antidepressants?
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If challanged with dexamethasone and unable to suppress cortisol these patients are likely to have a poor response
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True or False:
Patients with depression have thyroid abnormalities |
True
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How would you treat mild - moderate Major Depressive Disorder?
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Antidepressants or pyschotherapy
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How would you treat severe Depressive Disorder?
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Antidepressants and pyschotherapy
Electroconvulsive therapy - works very well if pyschotic features are present |
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"Treatment resistant depression" is treated with
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-Change the class of drugs
-ECT -Antidepressants & Lithium or thyroid hormone -Vagal nn stimulation |
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What is a mood stabilizer?
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Treatment that will treat/ prevent both episodes of mania or depression and not increase the likelihood of the opposite mood state
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Name the three main categories of mood stabilizers:
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Lithium
Certain Anticonvulsants - Valproic acid, carbamazepide, lamotrigine Second generation antipyschotics- Aripiprazole, Olanzapine, Quetiapine, risperidone, Ziprasidone |
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What is the controversy about the treatment of Bipolar disorder with antidepressants?
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Thoug frequently used, they are thought to have ltd efficacy and may worsen the course of illness or switch to mania.
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You are treating a patient with unipolar depression with antidepressants, what do you need to know as a physcian?
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All antidepressants probably work as first
2nd line antidepressants are most frequently used (SSRI's). First line antidepressants are used for recurrent htn. If patients recover, use the same dose that worked for an additional 6-12months, NOT LESS. |
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with 2 episodes of unipolar depression with antidepressants, what do you need to know as a physcian?
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Continue treatment for prophylaxis for 5 years
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with 3 episodes of unipolar depression with antidepressants, what do you need to know as a physcian?
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Continue treatment for prophylaxis indefinately
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List the 6 SSRI's found in the US
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Sertraline
fluoxetine Paroxetine Citalopram Escitalopram Fluvoxamine |
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The only treatment of bipolar disorder shown to reduce the risk of suicide is:
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Lithium
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Can Lamotrigine be used to treat bipolar disorder?
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Yes, can treat depressive and manic disorders in depression.
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This atypical antidepressant affects both DA and Noradrenergic receptors?
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Buproprion
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This a pre-synaptic alpha-2 blocker antidepressant, that increases release of 5HT and NE?
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Metaprazon
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What is the duration of acute treatment of depression?
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3wks - 6 wks, not less because it takes the medication about 2 wks to reach steady state and takes 6-8wks for marked benefit.
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If one has 3 episodes of depression, what is the likelihood that they will get another?
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90%, if 2 episodes 80% and if 1 episode, 50%
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Risk of a child of parent with bipolar disorder having a child with bipolar?
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10%
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Both parents with bipolar disorder, risk of children having bipolar?
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50%, advise patients on this
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What NT are involved in the pathophysiology of ADHD?
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NE and DA, prefrontal cortex (cognitive function and planning)
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What drugs are effective in the treatment of attentional & impulsivity symptoms in ADHD patients?
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Amphetamine stimulatants:
Methylphenidate - Ritalin Dexmethylphenidate Mized amphetamine salts Antidepressants Buproprion Venlaxafine TCA - amitryptiline, desipramine and nortriptyline Non-amphetamine stimulants Atomoxetine |
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Drugs ysed to treat hyperactivity symptoms in ADHD patients:
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Alpha-2 agonists:
Clonidine Guanfacine |
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Which drugs can be used to control tics worsened by stimulants in ADHD?
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Alpha-2 agonists:
Clonidine Guanfacine |
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Schizophrenia:
What % of population has this and what is the lifetime suicide rate of this patients? |
1% of patients
10 - 15% suicide rate |
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Etiology associated with Schizophrenia
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Genetic
Dopamine agonists - exacerbate positive symptoms DLPFC - injury causes apathy and negative symptoms |
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DSM IV criteria to diagnose schizophrenia
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Duration of illness = 6 months
Should have at 2 of the following positve symptoms for a continuous period of 1 month: Delusions Hallucinations Thought disorder Disorganized behavior Negative symptoms & this should affect their functioning |
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The most important complication of anorexia
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Death in 8 - 18% patients - primarily by arrythmia and suicide
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Patient refuses to maintain weight above 85%IBW, has missed 3 consecutive periods, has problems with her body image and intense fea of gaining weight
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Anorexia Nervosa, Restrictive or purging
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Patient has had recurrent binge eating and purging for @LEAST TWO DAYS A WK/3MONTHS. Also has problems with body image. What is Dx?
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Bulimia Nervosa
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What drug is indicated in the Rx of Bulimia nervosa?
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SSRI's
Fluoxetine - treat depression that is evident in many bullimic patients |
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When do you admit an anorexic patient
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If either:
<70%IBW Orthostatic/ bradycardic hypokalemic hypoglycemic |
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Lab findings in anorexic patients:
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All decreased except increase in cholesterol and carotene levels
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ECG findings in anorexic patients:
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QT prolongation
Sinus Bradycardia Non-specific T-wave abnormalities |
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Lab findings in Bulimia nervosa patients:
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Hypokalemic
Hypochloremic Decr. Plasma and phosphate levels |
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How do you treat excessive daytime somnolence in patients with narcolepsy?
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Stimulants:
- Modafinil - Methylphenidate |
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How do you treat REM symptoms in patients with narcolepsy?
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Antidepressants (SSRI - fluoxetine and TCA-Clomipramine)
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List drugs tha are used to treat insomnia
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Hypnotics - BZs and Zolpidem and Zaleplon
OTC antihistamines - Diphenhydramine Valerian - muscle relaxant and anxiolytic Melatonin |
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List Sedating antidepressants
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Amitriptyline
Doxepin Trimipramine Nefazodone Mirtazapine(Remeron) |
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Activating antidepressants:
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Protriptyline
Buproprion Most SSRI's Venlafaxine MAOI |
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What Rx would you offer one with advanced sleep phase syndrome (evening sleepiness)
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PM phototherapy
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What Rx would you offer one with delayed sleep phase syndrome (evening sleepiness)
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AM phototherapy
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What drug may be used to treat sleepwalking
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Clonazepam.
(These patients sleep walk in first third of night during non-REM sleep) |
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Difference between sleep terror and nightmares?
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Sleep terror is during NON-REM delta sleep whereas
Nightmares are during REM - cause abrupt wakening |
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REM sleep disorders with excessive movement may be treated with?
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Clonazepam
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Aqueous humor is drained to ciliary veins via?
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Canal of Schlemm
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Which organ makes acqueous humor?
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Ciliary body
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Where in the eye do you find Bruch's membrane?
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Between the retina and the choroid
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What type of epithelium is found in on the ciliary body and which cell layer (inner or outer is pigmented - note that both layers are part of retina)
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Stratified cuboidal epithelium
Outer layer - pigmented |
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Which cells of ciliary body generate the aqueous humor?
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Cells of the inner epithelium
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What is the name given to the fibers made of fibrillin that extend from the ciliary processes of eye to lens and form the suspensory ligament of the lens?
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Zonule fibers
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What effect does reduced tension of zonular fibers have on the lens?
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Accomodation
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What is the name given to the anterior surface of the iris?
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Anterior border layer - this does not have epithelium - condensation of fibroblasts and melanocytes
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Part of the retina that forms the outer layer in the iris has radially oriented muscles known as
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Dilator pupillae muscles
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The smooth muscle cells found in the center of the iris and involved in regulating pupil size are:
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Annular sphincter pupillae muscles
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These are specialized glial cells form the outer and inner limiting membranes of the retina and offer support to ganglion cells:
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Muller cells
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Define "watershed zone" with reference to the eye:
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Area between retinal and choroidal circulations
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