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Block 6 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is the main opioid receptor out of the three known?

A
  1. u - opioid receptor
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2
Q

What are the overall effects of opioid analgesics? [sedative, analgesic, amnesic, etc]

A

sedative and analgesic

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3
Q

When do withdrawal sx of opioids start?

A

6-12 hours after last dose

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4
Q

What occurs when opioid analgesic activates u opioid receptor? (3)

A
  1. u opioid receptor interacts with G protein to change ion channel gating
  2. In neurons, opioid agents cause opioid receptors to open K+ channels → hyperpolarization (less pain signals)
    • also causes closer of VG Ca2+ channels → this is on presynaptic neuron so NT are not released
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5
Q

How do opioids affect bowel movements?

A
  1. many u opioid receptors are located in GI tract → opioid agents cause delayed stool transit, increased water reabsorption, and overall constipation

at times opioids can be used to tx diarrhea

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6
Q

List some common
1. full u agonists
2. partial u agonists
3. opioids used for withdrawal sx

A
  1. fentanyl, morphine, codeine, methadone, hydrocodone, heroin, oxycodone, opium, etc
  2. buprenorphine, nalbuphine, butorphanol (“bu”)
  3. methadone, buprenorphine
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7
Q

List some common drugs that are
1. u antagonists
2. opioids used for diarrhea (do not cross BBB, have no analgesic properties)

A
  1. naloxone (narcan), naltrexone
  2. loperamide, diphenoxylate
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8
Q

Do opioids cause miosis or mydriasis?

A

miosis (pupil constriction)

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9
Q

What are the sx seen with opioid withdrawal

A

Rhinorrhea, Lacrimation, Yawning, Hyperventilation, Hyperthermia, Muscle aches, Vomiting, Diarrhea, Anxiety → **moist symptoms **

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10
Q

Why are methadone and buprenorphine used to help with opioid withdrawal sx?

A
  1. they have long half lives so when tapered off they don’t have extreme sx and are easier to manage for a pt

buprenorphine is partial u agonist ; methadone is full u agonist

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11
Q

What drug can mimic parkinson’s disease?

A

MTMP - it can destroy dopamine neurons and lead to drug induced parkinson’s

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12
Q

How does levodopa cause beneficial changes to patient with parkinsons? (MOA)

A
  1. Levodopa is precursor to dopamine and CAN cross BBB (unlike dopamine)
  2. Once inside brain/CNS, DOPA decarboxylase converts levodopa into dopamine for CNS use
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13
Q

Why is Carbidopa given with levodopa for parkinson’s patients

A
  1. DOPA decarboxylase converts levodopa into dopamine both in and outside the CNS.
  2. Since carbidopa doesn’t cross BBB - it works outside the CNS to inhibit DOPA decarboxylase and increase bioavailability of levodopa
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14
Q

What is the purpose of Entacapone and Tolcapone in parkinsons treatment?

A
  1. COMT converts levodopa to 3-OMD (thus decreasing levodopa bioavailability)
  2. Both of these drugs inhibit COMT
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15
Q

When is entacapone or tolcapone used over carbidopa

A
  1. usually tolcapone and entacapone are given after patient has used levodopa and carbidopa and is starting to experiencing on-off syndrome and wearing off reaction
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16
Q

What is the difference between entacapone and tolcapone?

A
  1. tolcapone works in both peripheral and central COMT
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17
Q

Major side effect of tolcapone that can make providers favor entacapone?

A
  1. hepatic failure
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18
Q

Side effects of levodopa?
1. with too much in periphery
2. too much centrally
3. chronic levodopa use (2)

A
  1. GI distress, N/V, cardiac arrhythmias, orthostatic hypotension
  2. Neurospychiatric sx like anxiety, agitation, insomnia, confusion, hallucinations
  3. Wearing off rx (at end of each dose) and on-off phenomenon (periods of akinesia with periods of improved mobility)
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19
Q

Why is levodopa contraindicated in psychiatric patients?

A

levodopa is contraindicated in psychotic patients because the method of treating psychotic patients is blocking CNS dopamine (too much dopamine in psychotic patients)

ex: schizophrenia

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20
Q

How is selegiline used for in parkinsons patients?

A

MOA: increases availability of dopamine in CNS by inhibiting MAO-B, which increases dopamine

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21
Q
  1. How is ropinirole used for in parkinsons patients?
  2. Side effects
A
  1. MOA: D2 dopamine receptor agonist
  2. can enhance impulse control disorders like gambling, shopping, hypersexuality
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22
Q
  1. How is pramipexole used for in parkinsons patients?
  2. Side effects
A
  1. MOA: D3 dopamine receptor agonist - an important initial tx
  2. can enhance impulse control disorders like gambling, shopping, hypersexuality
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23
Q
  1. How is amantadine used for in parkinsons patients?
  2. Why is it not used over levodopa
A
  1. MOA: enhances the effect of endogenous dopamine by increasing its synthesis/release and inhibiting its re-uptake
  2. Can alleviate dyskinesia sx but not as effective as levodopa and effects are short lived. Added as adjunctive to levodopa.
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24
Q
  1. How is trihexyphenidyl and benztropine used for in parkinsons patients?
  2. What sx does it improve and NOT IMPROVE in parkinsons?
  3. Side effects?
A
    • MOA: Antimuscarinic agents used to tx parkinsons
      -> parkinson’s shows less dopamine in substantia nigra and with it unbalanced high levels of ACh → these drugs can balance out the effects of ACh to what dopamine can do on basal ganglia
  2. Improve tremor and rigidity of Parkinson’s but no effect on bradykinesia
  3. Memory issues
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25
Q

suffix of local anesthetics

A

-caine

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26
Q

How do you differentiate from name of drug if local anesthetic is amide or ester?

A
  1. amides have to i’s in the name like lidocaine, mepivacaine, etc
  2. esters have only one i like procaine, cocaine, tetracaine
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27
Q

What is the mechanism of action of local anesthetics? (3)

A
  1. local anesthetics are weak bases so in their uncharged form it can cross the cell membrane
  2. Inside the cell it binds to H+ to become charged
  3. Charged form is able to blocking OPEN STATE voltage gated Na+ channels - prevents depolarization to occur
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28
Q

Side effects of local anesthetics are uncommon but some can appear such as in…
1. CNS
2. Cardiovascular
3. Neurons/neurology
4. Blood

describe each side effect

A
  1. Initially cause stimulation (talkative, anxiety) and later can cause drowsiness
  2. Hypotension, arrhythmia, bradycardia, heart block
  3. Nerve injury if directly injecting drug into nerve
  4. amount of oxygen carried through blood is greatly reduced (hemoglobin can carry oxygen but is not able to release it effectively)
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29
Q

Cardiovascular side effects of local anesthetics usually are hypotension, bradycardia, and heart block but how is cocaine an exception to this?

A
  1. cocaine leads to hypertension and vasoconstriction
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30
Q

What local anesthetics cause methemoglobinemia (where hemoglobin is not able to release oxygen effectively)?

A
  1. prilocaine and benzocaine
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31
Q

Propofol
1. What type of drug?
2. MOA

A
  1. IV anesthetic
  2. Potentiate chloride current through the GABA-A receptor complex
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32
Q
  1. What effect does propofol have on anesthesia?
  2. What side effects can occur?
A
  1. induction and maintenance of anesthesia
  2. profound vasodilation -> hypotension
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33
Q

Etomidate
1. What type of drug?
2. MOA?
3. Benefit of this drug?

A
  1. IV anesthetic
  2. Potentiate Cl current through GABA-A receptor complex
  3. Preserves cardiovascular stability
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34
Q

Ketamine
1. What type of drug?
2. MOA

A
  1. IV anesthetic
  2. Inhibits NMDA receptor complex (which is usually activated by excitatory glutamate)
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35
Q

Affects on anesthesia by etomidate drug?

A
  1. for induction of anesthesia
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36
Q
  1. Affects on anesthesia by ketamine?
  2. Side effects?
A
  1. induction of anesthesia
  2. Dissociative anesthesia (eyes open with nystagmic gaze), unpleasant hallucinations, CV stimulation
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37
Q

When is benzodiazepines used as anesthetic?

A
  1. for conscious sedation for minor procedures (like colonoscopy)
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38
Q
  1. When is barbiturates used as anesthetic?
  2. What barbiturate is fast acting
A
  1. used for induction of anesthesia
  2. Thiopental - 5 to 10 minutes
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39
Q

Nitrous oxide
1. What kind of drug is this
2. pharamacokinetics in blood? (solubility in blood, onset of action, rate of recovery)

A
  1. inhaled anesthetic (laughing gas)
  2. less soluble in blood means gas will saturate the blood faster and partition into tissue -> faster onset of action.
    - faster rate of recovery
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40
Q

Halothane
1. what kind of drug is this
2. pharamacokinetics in blood? (solubility in blood, onset of action, rate of recovery)

A
  1. inhaled anesthetic
  2. highly soluble in blood so slower onset of action and longer recovery
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41
Q

What does MAC mean for inhaled anesthetics?

A

the dose of anesthetic that causes 50% of patients to become unresponsive to painful stimuli

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42
Q

How can you determine potency of an inhaled anesthetic with MAC?

A

1/MAC

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43
Q

What are some side effects of inhaled anesthetics?
1. cardiovascular
2. pulmonary
3. blood
4. liver
5. kidney
6. muscle

A
  1. myocardial depression
  2. respiratory depression
  3. increased cerebral blood flow that can increase ICP
  4. Halothane can cause hepatotoxicity
  5. Enflurane can cause nephrotoxicity and seizures
  6. malignant hyperthermia
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44
Q
  1. What is malignant hyperthermia
  2. What can help treat this?

Can be a side effect of inhaled anesthetics

A
  1. Defective RyR releases excessive Ca2+ when introduced to anesthetic → leads to excessive ATP uptake by SR ⇒ lots of heat production (hyperthermia)
    • This induces muscle damage (rhabdomyolysis)
  2. Dantrolene (muscle relaxant)

succinylcholine can also cause this side effect

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45
Q

Amyotraphic Lateral Scleroris (ALS) - Lou Gherig’s Disease
1. Pathophysiology
2. Does it show UMN or LMN sx?

A
  1. neurodegenerative disease - progressive degeneration of nerve cells of spinal cord and brain.
  2. Both - UMN (corticobulbar/corticospinal) and LMN (medullary and spinal cord) degeneration. No sensory or
    bowel/bladder deicits.
    -> LMN deicits: laccid limb weakness, fasciculations,
    atrophy, bulbar palsy (dysarthria, dysphagia,
    tongue atrophy).
    -> UMN deficits: spastic limb
    weakness, hyperrelexia, clonus, pseudobulbar palsy
    (dysarthria, dysphagia, emotional lability).
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46
Q

ALS
1. what sx ultimately leads to death?
2. what tx is given for ALS?

A
  1. respiratory failure
  2. riluzole - not a cure but may extend survival
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47
Q

NMJ - where motor neuron meets what?

A
  1. meets a muscle fiber and causes muscle contraction
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48
Q

Myasthenia Gravis
1. pathophysiology
2. sx

A
  1. autoimmune condition- antibodies against post synaptic ACh receptors
  2. Fatigable muscle weakness—ptosis; diplopia; proximal weakness; respiratory muscle involvement; dyspnea; bulbar muscle involvement, dysphagia, dificulty chewing
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49
Q

Lambert-Eaton Myasthenia Syndrome (LEMS)
1. Pathophsyiology
2. Sx
3. Appears with what other disease

A
  1. Antibodies against calcium channels in the presynaptic membrane to decrease ACh release (this is more rare than myasthenia gravis)
  2. Slow onset with symmetric proximal muscle weakness + Autonomic symptoms (dry mouth, constipation, impotence) + Hyporelexia (decreased or absent reflex response) Improves with muscle use
  3. Paraneoplastic syndrome that classically occurs in small cell lung cancer
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50
Q

What sx presentation differentiates LEMS from myasthenia gravis?

A
  1. LEMS - muscle use will improve symptoms
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51
Q

Dermatomyositis
1. pathophysiology
2. sx

A
  1. autoimmune muscle disorder - perimysial and perivascular inflammation + perifascicular atrophy due to upregulation of MHC1 proteins on muscle fibers
  2. Progressive proximal muscle weakness, Heliotrope rash (image), gottron papules, systemic complications, etc
52
Q

Emery-Dreifuss Muscular Dystrophy
1. what is this
2. sx

A
  1. Early contractures and slowly progressive muscle weaking/wasting -> can lead to fatal cardiac involvement
  2. flexure contractures, cardiomyopathy with conduction defects
53
Q

Colchicine Myopathy
1. What is it?
2. Sx
3. What labs present with this

A
  1. clinical weakness due to prolonged colchicine use
  2. myalgia and proximal weakness
  3. serum CK is very high
54
Q

dorsal column-medial lemniscus pathway
1. what information does it process
2. What direction does it go (peripheral to brain or brain to peripheral)
3. Where in the spinal cord is the tract found?

A
  1. fine touch, vibration, proprioception
  2. peripheral to brain
  3. posterior part of spinal card
55
Q

Spinothalamic Tract
1. what information does it process
2. What direction does it go (peripheral to brain or brain to peripheral)
3. Where in the spinal cord is the tract found?

A
  1. pain and temperature
  2. peripheral to brain
  3. Image (somewhat anterior, somewhat lateral)
56
Q

precentral vs postcentral gyri
Which one is which
1. Primary motor cortex
2. Primary somatosensory cortex

A
  1. precentral gyrus - primary motor cortex
  2. postcentral gyrus - primary somatosensory cortex
57
Q

Corticospinal Tract
1. what information does it process
2. What direction does it go (peripheral to brain or brain to peripheral)
3. Where in the spinal cord is the tract found?

A
  1. It carries movement-related information from the cerebral cortex to the spinal cord
  2. brain to peripheral
  3. lateral and anterior spots (image)
58
Q

Vestibulospinal Tract
1. Lateral VST -> function
2. Medial VST -> function

medulla and pons of the hindbrain

A
  1. Lateral VST -> Excites antigravity muscles, adjust posture to compensate body movements/tilts
  2. Medial VST -> innervates neck muscles in order to stabilize head position, involved in coordination of head and eye movements
59
Q

Reticulospinal tract
1. reticular formation (brainstem) -> function

A
  1. Regulate sensitivity of LMN reflexes
  2. Participates in the control of posture
  3. Lateral RST - facilitates flexors mainly
  4. Medial RST - excites extensors mainly
60
Q

Rubrospinal Tract
1. Where is the red nucleus?
2. Red nucleus -> function

A
  1. Midbrain
  2. Activation causes excitation of flexor muscles and inhibition of extensor muscles
61
Q

Positive Babinsky sign is a sign of UMN or LMN damage

A

UMN damage

62
Q

Decerebrate Rigidity
1. Damage to what causes this?
2. What are the symptoms

A
  1. lesion at or below red nucleus
  2. presents with extension of upper and lower extremities
63
Q

Decorticate Rigidity
1. Damage to what causes this?
2. What are the symptoms

A
  1. lesion above red nucleus
  2. presents with flexion of upper extremities and extension of lower extremities
64
Q

Meissner Corpuscles
1. What type of tactile discrimination does this identify

A
  1. light touch
65
Q

Merkel disc
1. What type of tactile discrimination does this identify

A
  1. light touch
66
Q

Ruffini Corpuscles
1. What type of tactile discrimination does this identify

A
  1. sensitive to skin stretch
67
Q

Pacinian Corpuscles
1. What type of tactile discrimination does this identify

A
  1. sensitive to vibration
68
Q

Aβ, Aδ, C nerve fibers
1. Which one is largest (most myelinated) and smallest diameter
2. Which has fastest and slowest conduction velocity
3. What info does each typically conduct

A
  1. Aβ has largest diameter/most myelinated —- C fibers has smallest diameter/least myelinated
  2. Aβ has fastest conduction velocity —- C fiber has slowest conduction velocity
  3. Aβ - touch; Aδ, C - pain
69
Q

Nociception vs pain

A
  1. Nociception - sensory process that provides signals that trigger pain - does not necessarily lead to conscious perception of pain
  2. Pain - perception or feeling of nociception signals as irritating, sore, stinging, etc
70
Q

First pain vs Second pain
1. What is the difference between the two
2. What fibers coordinate this pain

A
  1. 1st pain - acute “sharp” pain;;; 2nd pain - dull burning type pain
  2. 1st - Aδ —- 2nd - C fibers
71
Q

Hyperalgesia

A

An increased sensitivity to feeling pain and an extreme response to pain

72
Q

Allodynia

A

Pain due to a stimulus that does not normally provoke pain

73
Q

Endorphins binds to opiate receptors and block release of (blank) - involved in pain responses

A

substance P

74
Q
  1. What is chorea/dyskinesia?
A
  1. random, purposeless, unpredictable brief movements that flow from one body part to another - seems like dancing
75
Q

Levels of dopamine in relation to
1. Hypokinetic disorders
2. Hyperkinetic disorders

A
  1. Hypo - lack of dopamine
  2. Hyper - abundance of dopamine
76
Q

Parkinson’s Disease
1. Degeneration of what?
2. How does this appear in gross anatomy
3. Hallmark in histology

A
  1. substantia nigra (specifically pars compacta)
  2. loss of brown color of substantia nigra
  3. Lewy bodies composed of alpha syn-nuclein (in SN)
76
Q

Parkinson Disease
1. What sx occur (TRAPSS)

A

T- Tremor (pill-rolling tremor at rest)
R- Rigidity (cogwheel)
A- Akinesia (or Bradykinesia)
P- Postural instability
S- Shuffling gait
S- Small handwriting

77
Q

Dystonia

A
  1. Dystonia is a movement disorder that causes the muscles to contract involuntarily. This can cause repetitive or twisting movements.
78
Q
  1. Ballismus
  2. How is this different from chorea
A
  1. A severe movement disorder that is characterized by spontaneous involuntary movements, muscular weakness and incoordination of movements of the proximal extremities
  2. Chorea is dance like but ballismus is violent flinging movement. Chorea is more on distal movements and ballismus is more on proximal movements.
79
Q

Huntington’s Disease
1. Genetic mutation
2. Degeneration of what
3. Changes in levels of what NTs (3)
3. Presentation in gross imaging

A
  1. CAG trinucleotide repeat
  2. Striatum (caudate and putamen)
  3. Loss of GABA and ACh; Increase in Dopamine
  4. Atrophy of caudate and putamen with ex vacuo ventriculomegaly.
80
Q

Huntington’s Disease
1. symptoms
2. Onset

A
  1. Chorea, dementia, aggression, and depression
  2. 30s-40s
81
Q

Huntington’s Disease
1. What treatment can be given
2. What are their MOA

A
  1. Block dopamine vesicle packaging -> tetrabenazine and reserpine
  2. Dopamine receptor antagonist -> Haloperidol
82
Q

Progressive Supranuclear Palsy (Atypical Parkinsonisms)
1. What is it?
2. Symptoms
3. Often mistaken for what and why

A
  1. Eye movement abnormalities which lead to falls (can’t look down which causes falls)
  2. Prominent postural instability (frequent falls), emotional incontinence, muscle stiffness, slow/quiet/slurred speech
  3. Alzheimers bc taupathy is seen
83
Q

Progressive Supranuclear Palsy (Atypical Parkinsonisms)
1. What changes are seen in imaging

A
  1. Midbrain becomes thin and resembles humming bird
84
Q

Corticobasal Degeneration (Atypical Parkinsonism)
1. What is it?
2. Symptoms
3. Often mistaken for what and why

A
  1. A progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia
  2. Very Asymmetric Parkinsonism (limb dystonia), cognitive impairment, muscle jerk (myoclonus), alien limb, language problems
  3. Shows taupathy which is why it is confused for alzheimers sometimes
85
Q
  1. What is Parkinsonism
  2. What are the dx symptoms (need 2 out of 3 to dx)
A
  1. Parkinsonism is an umbrella term that refers to brain conditions that cause slowed movements, rigidity (stiffness) and tremors.
  2. Tremor, bradykinesia, rigidity
86
Q

Multiple System Atrophy (Atypical Parkinsonism)
1. Symptoms

A
  1. Dysautonomia - a lot of ANS problems like temp dysregulations (cold hands), hypertension issues, urinary complaints, early gait abnormality (cerebellar ataxia)
  2. Multiple systems affected
87
Q

Intention tremor vs Resting tremor vs Essential tremor

A
  1. Tremors that occur with intentional movement
  2. Tremor at rest and alleviated with intentional movement
  3. Can occur with rest, can worsen with intentional movement or anxiety
88
Q

Wilson’s Disease
1. Pathophysiology
2. dysfunction of what anatomical location
3. Symptoms

A
  1. Disorder of copper metabolism - accumulation of copper in tissues
  2. GP internus and striatum
  3. Parkinsonian, wing-beating tremor (flapping of elbows), difficulty speaking
89
Q

Hemiballism
1. Where is the lesion found?
2. Sx

A
  1. Subthalamic Nucleus in Basal Ganglia
  2. Hyperkinetic movement disorder -> violent involuntary limb movements on one side of the body

Ballismus affects both sides of the body

90
Q
  1. What is the major function of basal ganglia
  2. What structures is it made up of? (5)
A
  1. Responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions.
  2. Substantia nigra, subthalamic nucleus, putamen, globus pallidus, caudate nucleus
91
Q
  1. Striatum is made up of (Blank A and Blank B)
  2. Lentiform nucleus is made up (Blank C and Blank D)
A
  1. putamen and caudate
  2. putamen and globus pallidus
92
Q

How is direct pathway altered in parkinson’s to show symptomology?

A
  1. Direct - Dopamine in SN is lost so cannot active D1 receptors in striatum (first part of direct pathway)
  2. loss of ability to initiate movement (bradykinesia)
93
Q

How is indirect pathway altered in parkinson’s to show symptomology?

A
  1. Loss of dopamine neurons results in increased activity in indirect pathway - strengthens indirect pathway (inhibition of movement)
94
Q

How is direct and indirect pathway altered in Hungtinton’s to show symptomology?

A

Huntington’s disease results from the selective loss of striatal neurons in the indirect pathway (Figure 4.10). Thus, the balance between the direct and indirect pathways becomes tipped in favor of the direct pathway.

95
Q

What are the three lobes of the cerebellum?

A
  1. Anterior
  2. Posterior
  3. Flocculonodular
96
Q

What are the three vertical sections of the cerebellum?

A
  1. Midline vermis
  2. Paravermis/intermediate hemisphere
  3. Lateral hemisphere
97
Q

What are the three functional zones of the cerebellum?

A
  1. Spinocerebellum
  2. Cerebrocerebellum
  3. Vestibulocerebellum
98
Q

Vertical sections of cerebellum
1. Function of vermis
2. Function of intermediate hemisphere

A
  1. coordinates midline movements and eye movemets
  2. coordinates distal muscles
99
Q

Functional zones of cerebellum
1. Function of spinocerebellum
2. Function of cerebrocerebellum
3. Function of vestibulocerebellum

A
  1. regulates gross limb movements
  2. regulates fine movements of distal limbs
  3. regulates postural equilibrium and eye movements
100
Q

What are the three deep nuclei of the cerebellum?

A
  1. Dentate
  2. Fastigial
  3. Interposed nucleus (emboliform and globose)
101
Q

What are the three peduncles of the cerebellum?

A
  1. superior
  2. middle
  3. inferior
102
Q

What are the three cortical layers of the cerebellum?

A
  1. molecular
  2. purkinje
  3. granular
103
Q
  1. What is the purpose of the cerebellar peduncles?
  2. Which ones carry input vs output
  3. input from where and output from where
A
  1. This is where information comes into the cerebellum and leaves
  2. Inferior and middle peduncles have afferent/input while superior has efferent/output
  3. Inferior - afferent fibers from the medulla; middle - afferents from pontine nuclei; superior- efferents from cerebellar nuclei to red nucleus and thalamus
104
Q

cortical layers of cerebellum
1. molecular (surface)
2. purkinje
3. granule (deep)

Describe what is found in them/purpose?

A
  1. Molecular - few cell bodies, mostly axons and dendrites of neurons whose cell bodies are in deeper layers
  2. Purkinje cell layer - Purkinje cells have inhibitory connections onto the cerebellar nuclei -> Purkinje are output of the cerebellar cortex but cerebellar nuclei are output of whole cerebellum
  3. Granule - granule cells receive info from mossy fibers and project to purkinje cells
105
Q

cerebellar lesions cause ipsilateral or contralateral manifestations?

A

ispilateral

106
Q
  1. Lateral lesions to cerebellum causes what general deficits
  2. midline lesions to cerebellum causes what general deficits
A
  1. voluntary movement of extremities with propensity to fall toward injured side
  2. affects movement of trunk, nystagmus, head tilting -> usually see bilateral motor deficits affecting axial and proximal musculature
107
Q

Poliomyelitis (Polio)
1. What part of the nervous system is affected
2. Symptoms?

A
  1. anterior horn -> affects LMN
  2. weakness in legs more than arms + LMN sx + infection sx and elevated WBC
108
Q

Werdnig-Hoffman Disease
1. Cuase and what is affected
2. Symptoms?

A
  1. Genetic condition that causes muscle atrophy
  2. Hypotonia and weakness in newborn, tongue fasciculations, “floppy baby” -> death of baby in few months
109
Q

Anterior Spinal Artery Occlusion
1. Symptoms initially?
2. Symptoms after a few weeks?

A
  1. Initial - spinal shock;; bilateral flaccid paralysis (loss of LMN) below lesion
  2. Weeks later some recover - since its a watershed area … Presents with UMN deficit below the lesion (corticospinal tract), LMN deficit at the level of the lesion (anterior horn), and loss of pain and temperature sensation below the lesion (spinothalamic tract).
110
Q

Tabes Dorsalis
1. A result of disease?
2. Pathology
3. Sx

A
  1. tertiary syphilis
  2. demyelination of posterior column (proprioception and vibration) and lose dorsal roots (no sensory input)
  3. difficulty walking, wide based gait, loss of reflexes
111
Q

Syringomyelia
1. pathophysiology
2. symptoms
3. where in body do sx present

A
  1. fluid filled space froms around spinal canal and damages spinothalamic nerves
  2. leads to bilateral loss of pain/temp sensation (since fluid is at point of desucation for pathway).
  3. Only at level of lesion/syrinx (usually C8-T1 which causes prick/temp loss on only hands/back)
112
Q

Subacute Combined Degeneration (SCD) or Vit B12 deficiency
1. pathophysiology
2. sx

A
  1. Demyelination of Spinocerebellar tracts, lateral Corticospinal tracts, and Dorsal columns.
  2. Ataxic gait, paresthesia, impaired position/vibration sense (⊕Romberg sign), UMN symptoms.
113
Q

Brown-Sequard Syndrome
1. pathophysiology
2. Explain the 3 big sx changes

A
  1. loss of half of spinal cord due to trauma or tumor
  2. At point of injury - complete sensory loss and motor function loss
  3. Below point of injury ipsilateral - loss of proprioception and vibration + UMN signs
  4. Below point of injury contralateral - loss of pain and temp info
114
Q

Cauda Equina Syndrome
1. Pathophysiology
2. Sx

A
  1. Compression of spinal roots L2 and below, often due to intervertebral disc herniation or tumor.
  2. Radicular pain, absent knee and ankle relexes, loss of bladder and anal sphincter control, saddle anesthesia.
  3. sx are gradual and unilateral
115
Q

Conus Medullaris Syndrome
1. pathophysiology
2. sx

A
  1. compression at L1-L2 specifically
  2. Presentation is sudden and bilateral with more low back pain, ankle jerks affected, numbness to perianal area
116
Q

What medication type is useful to treat essential tremor?

A
  1. beta blocker (like propanolol)
  2. if pt has COPD, heart block, tachycardia - use other med (like primidone - an anticonvulsant) due to contraindications

theres other drugs too and surgery like deep brain stimulation

117
Q

In the TMJ
1. what is the function of the lower compartment
2. What about the upper compartment?

A
  1. lower - hinge like movements of depression and elevation of mandible
  2. upper - gliding movments of protrustion and rectraction of mandible
118
Q

Function of posterior and anterior spinocerebellar tracts

A

The posterior and anterior spinocerebellar tracts are involved in nonconscious sensation of limb proprioception.

119
Q

Polymyositis
1. What is it?

A
  1. Progressive symmetric proximal muscle weakness, characterized by endomysial inlammation with CD8+ T cells.
  2. Most often involves shoulders.
  3. Polymyositis is an inflammatory myopathy characterized by degenerating, regenerating and necrotic muscle fibers, and endomysial inflammation.
120
Q

Differentiate which sections of spinal cord they are

A

image

121
Q

What is the fasciculus gracilis?

A
  1. Fasciculus gracilis carries sensory information associated with the DCML pathway from the lower extremities and terminates and synapses at the nucleus gracilis in the caudal medulla.
122
Q

What is the fasciculus cuneatus?

A
  1. Input from the arms
  2. fiber bundle that carries tactile and proprioceptive information from the upper limbs and torso, the fasciculus cuneatus is part of the dorsal columns and terminates in the nucleus cuneatus.
123
Q
  1. Purpose of VPL
  2. Purpose of VPM
    in the thalamus
A

VPL and VPM are the primary thalamic relays for somatic sensory, i.e., nociceptive and tactile/kinestetic, information from the body and the head, respectively

124
Q

In post synaptic nerve fibers, opioids modulate what channel?

A
  1. Potassium channel - cause leakage of potassium from inside the cells and hyperpolarize the membrane
125
Q

Internal capsule - what is found in
1. Anterior limb
2. Genu
3. Posterior limb

A
  1. Frontopontine fibers (project from the frontal cortex to the pons) and Thalamocortical radiations (connect medial and anterior nuclei of the thalamus to the frontal lobes)
  2. Corticobulbar tract - carries UMN from the motor cortex to the CN nuclei that govern muscle movement in face and neck
  3. Corticospinal fibers, sensory fibers ([dorsal] medial lemniscus and [spinothalamic] anterolateral system) from the body
126
Q

Symptoms of lesions to internal capsules

A

1.Weakness of the face, arm, and/or leg (pure motor stroke)
2.Upper motor neuron signs
3.Mixed sensorimotor stroke –> Since both motor and sensory fibers are carried in the internal capsule, a stroke to the posterior limb of the internal capsule (where motor fibers for the arm, trunk and legs and sensory fibers are located) can lead to contralateral weakness and contralateral sensory loss

Block 6 (9 decks)

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