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Neuroscience > Random Shit Of Week 4 > Flashcards

Random Shit Of Week 4 Flashcards

0
Q

Neurotransmitters and receptors for sympathetic?

A

Preganglionic: ACh on nicotinic receptors

Postganglionic: NE on adrenergic receptors (smooth muscles, glands) / ACh on muscarinic receptors ( sweat glands)

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1
Q

3 brainstem control centers

A

Respiratory - respiratory rate
Cardiovascular - BP
Micturition - urinary bladder distention

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2
Q

Neurotransmitters and receptors for parasympathetic?

A

Preganglionic: ACh on nicotinic

Postganglionic: ACh on muscarinic (smooth muscle, glands)

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3
Q

Sympathetic pathway of adrenal medulla

A

Preganglionic releases ACh on nicotinic receptors of adrenal medulla, releasing E (80%)or NE to circulation

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4
Q

Varicosities

A

Swellings of axon of postganglionic neuron

Function like a nerve terminal - synapses

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5
Q

Key regions that control ANS

A

Brainstem

Hypothalamus

Limbic system

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6
Q

Brainstem control of ANS

A

NST
Receives sensory info from CN 9,10
Coordinates reflexes
Relay info to hypothalamus

Reticular formation
Integrator - Receives sensory info from CN 9,10, Relay info to hypothalamus

PSNS Preganglionic nuclei
EW - III - pupillary reflex
Superior and inferior salivary - salivary reflex
Dorsal motor nucleus of vagus - X - lungs and GI
NA - IX, X - swallowing reflex, HR

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7
Q

Hypothalamus in ANS

A

Homeostatic function
Drive driven behavioral responses
Modulate nervous and endocrine system

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8
Q

How does hypothalamus monitor homeostatic function?

A

Senses directly by receptors near CVOs - neural signals

Transmits signal to hypothalamus

Effects change through neural signals and secretory CVOs (hormones)

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9
Q

Limbic system of ANS

A

Fight or flight/ fear response

Key structures: hippocampus, cingulate gyrus, anterior thalamic nuclei

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10
Q

Whats is the 3rd division of ANS?

A

Enteric nervous system
- function autonomously/ controlled by CNS through SNS and PSNS fibers

  • consists of myenteric and submucosal plexuses surrounding GI tract
  • neurons in plexuses are viscerosensory, interneurons, visceromotor neurons
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11
Q

General features of ANS dysfunction

A

Impaired pupillary reflex
Postural hypotension - light headedness, syncope, weakness, exercise intolerance
Deficient sweating (sudomotor) thermoregulation
GI dysfunction - impaired salivary ouput, early satiety, constipation, diarrhea
Hypoglycemic unawareness
Bladder dysfunction
Impotence:(

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12
Q

Clinical assessments of ANS

A

Cardio vagal
-orthostatic test, tilt table test, valsalva maneuver, HR with respiration

Sudomotor
- TST, QSART

Other modalities

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13
Q

Stages of normal sleep

A

N1 - lightest stage

N2 - largest percentage of sleep, benzodiazepine increases this stage at expenses of N3

N3 - deep/ slow wave sleep, decrease with age, hard to wake someone up, decreases over the course of the might

REM - vivid dream state, phasic (burst of REM, increased in sympathetic - twitching) and tonic (low muscle tone), increases during night

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14
Q

Primary features of REM

A

Rapid eye movement
Atonia
Active EEG pattern

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15
Q

Epworth sleepiness scale

A

Measure amount of daytime sleepiness

0-24 score - higher the score higher the daytime sleepiness

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16
Q

3 criteria for insomnia

A

Difficulty initiating sleep, difficulty maintaining sleep, waking up too early

DESPITE adequate opportunity and circumstances for sleep

Short term - < 3 months
Chronic - 3-5 times a week for >3 months

Impaired of daytime function for the diagnosis is needed

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17
Q

Consequences of insomnia

A 
Cardiovascular morbidity - HTN, MI, CV disease, coronary heart disease
Immunosuppression
Obesity
Diabetes mellitus II
Depression, anxiety, drug abuse
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18
Q

Sleep deprivation

A

Sleep is insufficient causing problem with alertness and performance

Due to reduced quantity and quality

Acute
Chronic

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19
Q

Coma cocktail

A

Thiamine
Oxygen
Naloxone
Sugar

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20
Q

Similarities and differences between NREM and REM

A 
Similarities:
Body temp and metabolism decrease
Parasympathetic tone increases
Sympathetic tone decreases
GH increases
Prolactin increases
TSH decreases

Difference:
REM - muscle atonia except eyes and diaphram

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21
Q

3 types of sleep disorders

A

Sleepy
Cant sleep
Go bump in the night

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22
Q

Pentad of narcolepsy

A 
Excessive daytime sleepiness
Cataplexy 
Hypnagogic hallucination
Sleep paralysis
Fragmented nocturnal sleep
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23
Q

What is the function of urea cycle?

A

Disposal of amino groups generated through amino acid catabolism

Liver takes ammonia and generates urea

Excreted by kidney

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24
Why do we need to dispose ammonia?
Ammonia is a potent neurotoxin!!!! Wahhhhhh
25
How does ammonia get transported to liver???
By glutamine (muscle) and alanine (skeletal muscle)
26
what enzyme does the first step of urea cycle involve?
mitochondrial enzyme carbamoyl phosphate synthase I
27
Why did patient have elevated orotate?
With a ornithine transcarbamoylase deficiency, there are excessive carbamoyl phosphate because the 1st step of urea cycle is still functioning. Those CP will leak out of mitochondria and enter the pyrimidine biosynthesis pathway which also required CP, but a different enzyme CPS II. And one of the products of this pathway is orotate!!!
28
Why is urine glutamine elevated?
With ammonia, glutamate is converted to glutamine - an alternative path for elimination of ammonia
29
Why is patient drowsy?
2 theories: - brain uses ammonia after crossing BBB to make glutamate from alpha ketoglutarate via glutamate dehydrogenase. this depletes alpha ketoglutarate in brain which slows TCA cycle, decreasing ATP synthesis - since glutamate is a neurotransmitter, increasing glutamate in the brain might alter neuronal signaling - NMDA receptors
30
How is ornithine transcarbamoylase deficiency inherited?
X linked recessive
31
What food should be avoided with OTC deficiency?
Protein
32
Relationship between ethanol and hypoglycemia
Alcohol leads to a large generation of NADH. Different pathways ( pyruvate to lactate/ oxaloacetate to malate) are favored in order to get rid of NADH. Gbuconeogensis is then compromised.
33
CNS and adrenergic Sx of hypoglycemia
CNS (impaired delivery of glucose to brain): confusion, aberrant behavior, HA, slurred speech, seizure, coma/death Adrenergic (mediated by E release) : anxiety, palpitation, sweating, tremor
34
Why is brain better at phosphorylating glucose during hypoglycemia than liver?
Hexokinase is more efficient than glucokinase - higher affinity
35
What counter regulatory hormones are triggers during hypoglycemia?
E Glucagon GH Cortisol
36
Hypoglycemia Tx
Conscious patient: OJ Unconscious: glucagon injection
37
What happened to water distribution during hyperglycemia?
Water move to ECF from cell to balance the glucose concentration Cell experience dehydration
38
Why does hyponatremia happen too?
Sodium concentration goes down when water goes to ECF, diluting the concentration Hypotonic hyponatremia
39
Sx of hyponatremia
Moderate: nausea, vomiting, malaise, HA Severe: diminished reflexes, convulsions, stupor, coma/death
40
Confusion
Slowing of thinking
41
Delirium
Misperception, may fluctuate
42
Obtundation
Reduced alertness
43
Stupor
Stunned, just barely not comatose
44
Spectrum of acutely altered consciousness
Confusion Delirium Obtundation Stupor
45
Structural or metabolic AAC
PE - motor findings EEG - not really helpful Imaging - can see structural causes History - KEY
46
Possible causes of agitated delirium/ seizures
Stimulants- cocaine/ amphetamines, organiphosphates, amanita muscaria Withdrawal of sedatives Inhibitory inhibitors - tricyclic antidepressants, isoniazid, some antibiotics, water hemlock Enhance CNS stimulation by allowing influx of +ions after activation of NMDA receptors, depolarizing the cells
47
5 GABA agonists - withdrawals of sedatives
``` Benzodiazepines Barbiturates Baclofen GHB BOoze ```
48
GHB
Classic day rape drug Structurally similar to GABA, causing hyper-polarization of cells - CNS depression Short lived anesthesia with flaccid areflexic coma Withdrawal causes agitated delirium
49
Causes of toxin induced coma
Too little stimulation - alpha 2 agonist - alpha 1 antagonist - glutamate antagonist Too much inhibition - opioids/ opiates - benzodiazepines/ barbiturates
50
What defines consciousness
Wakefulness - ascending arousal system: dorsolateral pontine tegmentum, paramedian midbrain Awareness - thalamo cortical and cortical connections
51
Characteristics of coma
Sleeplike - eyes closed unarousable Unresponsiveness
52
Which part of the brain is more susceptible to hypoxia?
Cortex and thalamus > brainstem
53
How long does coma last?
Max 4 weeks
54
What defines vegetative state?
Wakefulness without awareness Disorder of cerebral integration at the thalamocortical level
55
Characteristics of VS
Sleep wake cycle present Preserved breathing, cardiac, autonomic functions Eyes open, blink, and move, NO sustained fixation/tracking NO language expression/ comprehension Posturing, withdrawal, reflex movement, NOT sustained, reproducible or purposeful
56
How to diagnose VS
Bedside Dx, no lab test Dynamic process with confounding factors Examiner bias Inherent uncertainty
57
What is lock in syndrome
Stroke in lower pon Total quadriplegia No facial movement or speech Partial or total ophthalmoplegia Preserved level and content of consciousness
58
Characteristics of minimally conscious state
``` Any: Follow simple command Gestural or verbal yes/no Intelligible verbalization Purposeful behavior: smiling crying reaching objects sustained fixation ``` Can be variable and inconsistent
59
Predicting coma outcome
Low if: Absent pupillary response > 3 days Absent motor response > 3 days
60
Prognosis for VS
Anoxic worse Longer worse Older worse
61
Tx for MCS and VS
Neurorehabilitation Facilitate communication Medications: amantadine, levodopa, zolpidem Deep brain stimulation

Neuroscience (6 decks)

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