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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
Q

Why do we need to dispose ammonia?

A

Ammonia is a potent neurotoxin!!!! Wahhhhhh

25
Q

How does ammonia get transported to liver???

A

By glutamine (muscle) and alanine (skeletal muscle)

26
Q

what enzyme does the first step of urea cycle involve?

A

mitochondrial enzyme carbamoyl phosphate synthase I

27
Q

Why did patient have elevated orotate?

A

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
Q

Why is urine glutamine elevated?

A

With ammonia, glutamate is converted to glutamine - an alternative path for elimination of ammonia

29
Q

Why is patient drowsy?

A

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
Q

How is ornithine transcarbamoylase deficiency inherited?

A

X linked recessive

31
Q

What food should be avoided with OTC deficiency?

A

Protein

32
Q

Relationship between ethanol and hypoglycemia

A

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
Q

CNS and adrenergic Sx of hypoglycemia

A

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
Q

Why is brain better at phosphorylating glucose during hypoglycemia than liver?

A

Hexokinase is more efficient than glucokinase - higher affinity

35
Q

What counter regulatory hormones are triggers during hypoglycemia?

A

E
Glucagon
GH
Cortisol

36
Q

Hypoglycemia Tx

A

Conscious patient: OJ

Unconscious: glucagon injection

37
Q

What happened to water distribution during hyperglycemia?

A

Water move to ECF from cell to balance the glucose concentration

Cell experience dehydration

38
Q

Why does hyponatremia happen too?

A

Sodium concentration goes down when water goes to ECF, diluting the concentration

Hypotonic hyponatremia

39
Q

Sx of hyponatremia

A

Moderate: nausea, vomiting, malaise, HA

Severe: diminished reflexes, convulsions, stupor, coma/death

40
Q

Confusion

A

Slowing of thinking

41
Q

Delirium

A

Misperception, may fluctuate

42
Q

Obtundation

A

Reduced alertness

43
Q

Stupor

A

Stunned, just barely not comatose

44
Q

Spectrum of acutely altered consciousness

A

Confusion
Delirium
Obtundation
Stupor

45
Q

Structural or metabolic AAC

A

PE - motor findings

EEG - not really helpful

Imaging - can see structural causes

History - KEY

46
Q

Possible causes of agitated delirium/ seizures

A

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
Q

5 GABA agonists - withdrawals of sedatives

A 
Benzodiazepines
Barbiturates
Baclofen
GHB
BOoze
48
Q

GHB

A

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
Q

Causes of toxin induced coma

A

Too little stimulation

  • alpha 2 agonist
  • alpha 1 antagonist
  • glutamate antagonist

Too much inhibition

  • opioids/ opiates
  • benzodiazepines/ barbiturates
50
Q

What defines consciousness

A

Wakefulness
- ascending arousal system: dorsolateral pontine tegmentum, paramedian midbrain

Awareness
- thalamo cortical and cortical connections

51
Q

Characteristics of coma

A

Sleeplike - eyes closed

unarousable

Unresponsiveness

52
Q

Which part of the brain is more susceptible to hypoxia?

A

Cortex and thalamus > brainstem

53
Q

How long does coma last?

A

Max 4 weeks

54
Q

What defines vegetative state?

A

Wakefulness without awareness

Disorder of cerebral integration at the thalamocortical level

55
Q

Characteristics of VS

A

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
Q

How to diagnose VS

A

Bedside Dx, no lab test

Dynamic process with confounding factors
Examiner bias
Inherent uncertainty

57
Q

What is lock in syndrome

A

Stroke in lower pon

Total quadriplegia

No facial movement or speech

Partial or total ophthalmoplegia

Preserved level and content of consciousness

58
Q

Characteristics of minimally conscious state

A 
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
Q

Predicting coma outcome

A

Low if:
Absent pupillary response > 3 days
Absent motor response > 3 days

60
Q

Prognosis for VS

A

Anoxic worse
Longer worse
Older worse

61
Q

Tx for MCS and VS

A

Neurorehabilitation
Facilitate communication
Medications: amantadine, levodopa, zolpidem
Deep brain stimulation

Neuroscience (6 decks)

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