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N216 A/B > [216B] Neuro Part 1 > Flashcards

[216B] Neuro Part 1 Flashcards

1
Q

The brain only makes up __% of body weight, but requires __% of CO per minute and __% of all O2.

A

2% of body weight, 15% of CO per minute and 20% of all O2.

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2
Q

Can the brain store O2? Can it store nutrients?

A

No.

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3
Q

Why can’t CNS cells recover from damage/injury?

A

They lack centrioles for cellular repair.

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4
Q

CNS cells will begin to take damage after __ seconds without O2 and will begin to die after __-__ minutes.

A

10 seconds; 4-6 minutes.

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5
Q

List 4 sequelae of brain injury.

A
  1. Ischemia.
  2. Cerebral edema.
  3. Metabolic acidosis.
  4. Increased ICP.
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6
Q

What is a focal injury vs a global injury?

A

Focal: only affects one area of the brain.
Global: affects all areas of the brain.

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7
Q

List some global deficits that may result from global injury.

A

Altered consciousness. (ex: stupor, coma)
Altered VS.
Declining autoregulation (ex: loss of protective reflexes like blinking, urinating, defecating)

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8
Q

Consciousness is dependent on which 2 areas of the brain?

A

Cerebral cortex & reticular formation (RAS).

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9
Q

Low RAS activity leads to _______ awareness and wakefulness.

A

Decreased.

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10
Q

What are 2 possible pathological causes of low RAS activity?

A

Decreased perfusion.

Altered metabolic state (ex: metabolic acidosis).

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11
Q

List the 3 criteria for brain death.

A
  1. No motor responses.
  2. No brainstem responses (ex: gagging, coughing).
  3. Apnea when taken off a ventilator.
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12
Q

Pts in a vegetative state will maintain their ________ _______, but will have no _________________.

A

Maintain their brainstem reflexes (ex: sleep-wake cycle, can function enough to meet their basic needs like temp regulation).
Will not have awareness of self or their surroundings.

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13
Q

Differentiate between hypoxia and ischemia.

A

Hypoxia: tissue lacking O2.
Ischemia: lack of O2 delivery/waste removal to a tissue.

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14
Q

What may cause focal ischemia?

A

A CVA (affected area will depend on where the blood flow has been affected).

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15
Q

List 2 possible causes of global ischemia.

A
  1. Metabolic acidosis (ex: severe asthma attack, ketoacidosis).
  2. Loss of CO (ex: severe arrhythmia/MI).
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16
Q

Describe 2 consequences of electrolyte imbalances d/t global ischemia.

A
  1. Cerebral edema: lack of depolarization leads to intracellular retention of electrolytes (ex: calcium), causing fluid to shift into cells.
  2. Neurotransmitter imbalances: electrolyte dysfunction impacts signalling for neurotransmitter secretion/recycling.
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17
Q

Why might we see “watershed infarcts” as a result of global ischemia?

A

The body prioritizes blood flow to more important areas of the brain, resulting in heightened focal damage to lowered-flow regions.

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17
Q

What might cause brain tissue to take up more space in the cranial cavity?

A

Tumors.

Cerebral edema.

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18
Q

What might cause the blood component to take up more space in the cranial cavity?

A 
Overhydration (increased overall blood volume).
Brain bleed (hemorrhaging).
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19
Q

What might cause the CSF component to take up more space in the cranial cavity?

A

Obstruction of CSF flow (ex: hydrocephalus).

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20
Q

There may be a reduction in venous blood flow in the brain to compensate for other cranial cavity contents taking up more space. What might be a consequence of this?

A

Decreased transport/disposal of waste products - may lead to accumulation and possibly toxicity.

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21
Q

What is the normal range for ICP?

A

0-15 mmHg.

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22
Q

How do we calculate CPP (cerebral perfusion pressure)?

A

CPP = MAP - ICP.

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23
Q

CPP is the pressure required to:

A

perfuse the brain.

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24
Q

What is the minimum CPP? At what CPP and below would we consider it to be “profound ischemia”?

A

Minimum = 45 mmHg.

Profound ischemia at <40 mmHg.

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25
Q

What are the dangers of having increased ICP? What would be the S&S if this was severe?

A

Obstructions fluid flow & may displace/injure brain cells (brain herniaton).
S&S: Cushing’s triad (HTN, widened PP, bradycardia).

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26
Q

What are the 4 general steps in treating brain injuries?

A
  1. Treat the cause of the CNS event.
  2. Treat the high ICP/cerebral edema.
  3. Maintain VS.
  4. Preserve function & avoid secondary injury.
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27
Q

T/F: concussions have additive effects (the more concussions you get, the worse they’ll likely be) and this reflects in the S&S.

A

True :)

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28
Q

Encephalitis is infection of the:
Myelitis is the infection of the:
Encephalomyelitis is the infection of the:

A

Encephalitis: brain tissue (parenchyma).
Myelitis: spinal cord.
Encephalomyelitis: brain & spinal cord.

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29
Q

Which pathogen causing bacterial meningitis has the highest mortality?

A

Strep pneumoniae (pneomococcus).

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30
Q

Describe the pathology of meningitis.

A

Inflammation > BBB compromise > inflammation > capillary “leaking”, cerebral edema, vascular congestion, cell death > meningeal thickening/adhesions = vascular congestion & decreased CSF outflow.

31
Q

What are 3 S&S that are almost exclusive to meningitis?

A
  1. Stiff neck (“nuchal rigidity”).
  2. Brudzinski sign (flexion of neck > flexion of hip & knee).
  3. Petechial rash.
32
Q

What drug classes do we use to treat meningitis? Which antibiotics are used?

A
  1. Broad spectrum antibiotics; 3rd gen cephalosporins, penicillins, vancomycin.
  2. Potent anti-inflammatory drugs (ex: glucocorticosteroids) for tx of inflammation.
33
Q

How do we classify the stages of brain tumors? Why does it differ from how we stage regular tumors?

A

Low-grade vs high-grade.
Different because other tumors will consider mestastasization as part of the staging criteria, but brain tumors are fairly unlikely to metastasize, so it’d be pointless to use those stages.

34
Q

What 3 treatments are used to treat brain tumors?

A

Surgery.
Radiation therapy.
Chemotherapy.

35
Q

Chemotherapy drugs are cidal to which types of cells?

A

Quickly replicating eukaryotic cells (ex: hair cells, GI cells, bone marrow cells, blood cells/platelets).

36
Q

Differentiate between idiopathic and symptomatic seizures.

A

Idiopathic: genetic origin w/ no known acquired cause (aka “epilepsy”) - tx with long-term anti-epileptic meds.
Symptomatic: d/t a brain injury (over-stimulation of neurons d/t altered action potential/neurotransmitter/electrolyte balance) - tx with short-term anti-epileptic meds & tx of underlying cause.

37
Q

Differentiate between the 3 main classes of seizure.

A

Focal: specific group of neurons in one hemisphere.
Generalized: both hemispheres involved.
Unknown: neither of the above (ex: febrile seizures in children).

38
Q

What are automatisms?

A

Repeating behaviours (ex: grimacing, lip smacking, patting).

39
Q

List 4 life-threatening seizure symptoms.

A
  1. Tonic convulsions causing constriction of muscles including the airway & diaphragm > respiratory distress.
  2. Loss of consciousness impairing respiratory rate/depth.
  3. Large convulsions can cause falls, flailing.
  4. Stimulation of ANS causes severe VS changes (ex: tachycardia, HTN, reflex hypotension, hyperventilation).
40
Q

Benzodiazepines are CNS _________ and enhance ______, an ________ neurotransmitter.

A

CNS depressants - enhance GABA, an inhibitory neurotransmitter.

41
Q

Why should pregnant/breastfeeding pts avoid benzodiazepines?

A

They will cross the placenta in pregnancy and the breast milk.

42
Q

What are the side effects of benzodiazepines?

A

Respiratory depression.
Drug-drug interactions.
Altered LoC/CNS activity (ex: amnesia).

43
Q

How do we treat benzodiazepine ODs?

A

Flumazenil (Romazicon): receptor antagonist.

44
Q

Benzodiazepines will generally end in:

A

-am/-pam.

45
Q

List 3 examples of benzodiazepines.

A

Clonazepam (Rivotril).
Diazepam (Valium).
Lorazepam (Ativan).

46
Q

Which 3 drug classes may be used as anti-epileptics?

A
  1. Benzodiazepines.
  2. Barbituates.
  3. Anticonvulsants.
47
Q

Barbituates are CNS _________ and enhance ______, an ________ neurotransmitter.

A

CNS depressants - enhance GABA, an inhibitory neurotransmitter.

48
Q

Are benzodiazepines or barbituates more addictive? Which tend to have a higher degree of tolerance?

A

Barbituates for both.

49
Q

How can we treat barbituate ODs?

A 
Activated charcoal.
Sodium bicarbonate (urinary alkalization).
50
Q

Barbituates often end in:

A

-barbital.

51
Q

List 3 barbituates.

A

Phenobarbital (Phenobarb).
Pentobarbital.
Secobarbital.

52
Q

Which benzodiazepine is often abused recreationally?

A

Alprazolam (Xanax).

53
Q

Which benzodiazepine is used for roofies?

A

Flunitrazepam (Rohypnol).

54
Q

Which barbituate may be used in euthanasia? What else may be used with it?

A

Secobarbital + antiemetics (ex: metoclopramide).

55
Q

Which benzodiazepine may be used in euthanasia? What else may be used with it?

A

Diazepam + paralytic agents (ex: Rocuronium) + anesthesia agents (ex: Propofol).

56
Q

How do anti-convulsants work?

A

Alter electrolyte (sodium or calcium) balance to delay action potential and decrease neuronal activity.

57
Q

Which anti-convulsants decrease sodium cellular influx?

A

Phenytoin (Dilantin).
Carbamazepine (Tegretol).
Valproic acid (Valproate).

58
Q

Why do we need to be extra cautious with pheytoin (Dilantin)?

A

It has a narrow TI and is highly PPB.

59
Q

List some side effects of anti-convulsants that decrease sodium cellular influx.

A

Arrhythmias (action potentials altered).
Drug-drug interactions.
Bleeding (d/t vit K interference).

60
Q

Why might a ketogenic diet be beneficial for seizure control?

A

Since no carbs (quick energy) are consumed in a ketogenic diet, the brain does not have easy access to glucose to fuel hyperactivity (it goes through a lot to even get the glucose it needs to function normally).

61
Q

What is status epilepticus?

A

When a seizure of any type progresses to an unstoppable state which becomes life threatening.
Medical emergency!!

62
Q

What is the first choice of treatment for status epilepticus?

A

Benzodiazepines (ex: diazepam, lorazepam) IV (NPO d/t respiratory depression).

63
Q

How do our brains synthesize melatonin?

A

Pinealocytes in the pineal gland use tryptophan (diet-acquired AA) to make serotonin, which is then converted to melatonin.

64
Q

Melatonin secretion is regulated via a feedback loop with the:

A

Hypothalamic SCN.

65
Q

Do older persons tend to produce more or less melatonin?

A

Less.

66
Q

Describe the steps in the onset of sleep.

A

Circadian rhythm + decreased RAS > decreased cortical stimulation = decreased excitatory neurotransmitter activity (ex: NE, acetylcholine) + increased inhibitory neurotransmitters (serotonin) + increased melatonin synthesis.

67
Q

What happens to our bodies during REM sleep?

A

Stage of muscle paralysis, altered VS, decreased BMR & cerebral blood flow; dreaming.

68
Q

How do the lengths of each sleep stage change as sleep time increases?

A

The longer you sleep, the longer REM stages will be and the shorter stages 3 and 4 of non-REM sleep will be (may even disappear completely, starting with stage 4).

69
Q

What are 5 factors that may increase a pt’s risk for insomnia?

A

Older age (decreased melatonin production).
Post-menopausal (r/t estrogen levels).
Co-morbidities (ex: pain).
Stimulant use (caffeine, nicotine, small amounts of ETOH).
Drug side effects (ex: glucocorticoids).

70
Q

What are the 4 primary types of treatments for insomnia?

A

Melatonin (synthetic).
Benzodiazepines - Flurazepam (Dalmane), Temazepam (Restoril), Triazolam.
Non-benzodiazepines - namely Buspirone (BuSpar).
Other: antihistamines (ex: diphenhydramine (Benadryl)), antidepressants.

71
Q

What is the mechanism of action for Buspirone (BuSpar)?

A 
Serotonin agonist (serotonin is an inhibitory, sedative neurotransmitter).
Dopamine 2 presynaptic binding (decreases post-synaptic dopamine, which is a precursor to stimulatory catecholamines).
72
Q

Is it safe to consume CNS depressants with other CNS drugs?

A

No >:0

73
Q

Which phase of sleep is obstructive sleep apnea most prevalent in? Why?

A

REM d/t muscle relaxation.

74
Q

What is the most prominent risk factor for sleep apnea?

A

Obesity (increased abdominal pressure > increased thoracic pressure = diaphragm motility decreased).

75
Q

What are the 3 types of anxiety?

A

Generalized anxiety.
Panic.
Social phobia.

76
Q

What are 3 ways to treat anxiety?

A 
Increase GABA (inhibitory) with benzodiazepines: Alprazolam (Xanax), diazepam (Valium), lorazepam (Ativan), midazolam (Versed).
Increase serotonin (inhibitory) while ensuring balance with SSRIs (selective serotonin re-uptake inhibitors).
Behavioural & cognitive therapies (counselling to improve coping).

N216 A/B (26 decks)

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