[216B] Neuro Part 1 Flashcards
The brain only makes up __% of body weight, but requires __% of CO per minute and __% of all O2.
2% of body weight, 15% of CO per minute and 20% of all O2.
Can the brain store O2? Can it store nutrients?
No.
Why can’t CNS cells recover from damage/injury?
They lack centrioles for cellular repair.
CNS cells will begin to take damage after __ seconds without O2 and will begin to die after __-__ minutes.
10 seconds; 4-6 minutes.
List 4 sequelae of brain injury.
- Ischemia.
- Cerebral edema.
- Metabolic acidosis.
- Increased ICP.
What is a focal injury vs a global injury?
Focal: only affects one area of the brain.
Global: affects all areas of the brain.
List some global deficits that may result from global injury.
Altered consciousness. (ex: stupor, coma)
Altered VS.
Declining autoregulation (ex: loss of protective reflexes like blinking, urinating, defecating)
Consciousness is dependent on which 2 areas of the brain?
Cerebral cortex & reticular formation (RAS).
Low RAS activity leads to _______ awareness and wakefulness.
Decreased.
What are 2 possible pathological causes of low RAS activity?
Decreased perfusion.
Altered metabolic state (ex: metabolic acidosis).
List the 3 criteria for brain death.
- No motor responses.
- No brainstem responses (ex: gagging, coughing).
- Apnea when taken off a ventilator.
Pts in a vegetative state will maintain their ________ _______, but will have no _________________.
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.
Differentiate between hypoxia and ischemia.
Hypoxia: tissue lacking O2.
Ischemia: lack of O2 delivery/waste removal to a tissue.
What may cause focal ischemia?
A CVA (affected area will depend on where the blood flow has been affected).
List 2 possible causes of global ischemia.
- Metabolic acidosis (ex: severe asthma attack, ketoacidosis).
- Loss of CO (ex: severe arrhythmia/MI).
Describe 2 consequences of electrolyte imbalances d/t global ischemia.
- Cerebral edema: lack of depolarization leads to intracellular retention of electrolytes (ex: calcium), causing fluid to shift into cells.
- Neurotransmitter imbalances: electrolyte dysfunction impacts signalling for neurotransmitter secretion/recycling.
Why might we see “watershed infarcts” as a result of global ischemia?
The body prioritizes blood flow to more important areas of the brain, resulting in heightened focal damage to lowered-flow regions.
What might cause brain tissue to take up more space in the cranial cavity?
Tumors.
Cerebral edema.
What might cause the blood component to take up more space in the cranial cavity?
Overhydration (increased overall blood volume). Brain bleed (hemorrhaging).
What might cause the CSF component to take up more space in the cranial cavity?
Obstruction of CSF flow (ex: hydrocephalus).
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?
Decreased transport/disposal of waste products - may lead to accumulation and possibly toxicity.
What is the normal range for ICP?
0-15 mmHg.
How do we calculate CPP (cerebral perfusion pressure)?
CPP = MAP - ICP.
CPP is the pressure required to:
perfuse the brain.
What is the minimum CPP? At what CPP and below would we consider it to be “profound ischemia”?
Minimum = 45 mmHg.
Profound ischemia at <40 mmHg.
What are the dangers of having increased ICP? What would be the S&S if this was severe?
Obstructions fluid flow & may displace/injure brain cells (brain herniaton).
S&S: Cushing’s triad (HTN, widened PP, bradycardia).
What are the 4 general steps in treating brain injuries?
- Treat the cause of the CNS event.
- Treat the high ICP/cerebral edema.
- Maintain VS.
- Preserve function & avoid secondary injury.
T/F: concussions have additive effects (the more concussions you get, the worse they’ll likely be) and this reflects in the S&S.
True :)
Encephalitis is infection of the:
Myelitis is the infection of the:
Encephalomyelitis is the infection of the:
Encephalitis: brain tissue (parenchyma).
Myelitis: spinal cord.
Encephalomyelitis: brain & spinal cord.
Which pathogen causing bacterial meningitis has the highest mortality?
Strep pneumoniae (pneomococcus).
Describe the pathology of meningitis.
Inflammation > BBB compromise > inflammation > capillary “leaking”, cerebral edema, vascular congestion, cell death > meningeal thickening/adhesions = vascular congestion & decreased CSF outflow.
What are 3 S&S that are almost exclusive to meningitis?
- Stiff neck (“nuchal rigidity”).
- Brudzinski sign (flexion of neck > flexion of hip & knee).
- Petechial rash.
What drug classes do we use to treat meningitis? Which antibiotics are used?
- Broad spectrum antibiotics; 3rd gen cephalosporins, penicillins, vancomycin.
- Potent anti-inflammatory drugs (ex: glucocorticosteroids) for tx of inflammation.
How do we classify the stages of brain tumors? Why does it differ from how we stage regular tumors?
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.
What 3 treatments are used to treat brain tumors?
Surgery.
Radiation therapy.
Chemotherapy.
Chemotherapy drugs are cidal to which types of cells?
Quickly replicating eukaryotic cells (ex: hair cells, GI cells, bone marrow cells, blood cells/platelets).
Differentiate between idiopathic and symptomatic seizures.
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.
Differentiate between the 3 main classes of seizure.
Focal: specific group of neurons in one hemisphere.
Generalized: both hemispheres involved.
Unknown: neither of the above (ex: febrile seizures in children).
What are automatisms?
Repeating behaviours (ex: grimacing, lip smacking, patting).
List 4 life-threatening seizure symptoms.
- Tonic convulsions causing constriction of muscles including the airway & diaphragm > respiratory distress.
- Loss of consciousness impairing respiratory rate/depth.
- Large convulsions can cause falls, flailing.
- Stimulation of ANS causes severe VS changes (ex: tachycardia, HTN, reflex hypotension, hyperventilation).
Benzodiazepines are CNS _________ and enhance ______, an ________ neurotransmitter.
CNS depressants - enhance GABA, an inhibitory neurotransmitter.
Why should pregnant/breastfeeding pts avoid benzodiazepines?
They will cross the placenta in pregnancy and the breast milk.
What are the side effects of benzodiazepines?
Respiratory depression.
Drug-drug interactions.
Altered LoC/CNS activity (ex: amnesia).
How do we treat benzodiazepine ODs?
Flumazenil (Romazicon): receptor antagonist.
Benzodiazepines will generally end in:
-am/-pam.
List 3 examples of benzodiazepines.
Clonazepam (Rivotril).
Diazepam (Valium).
Lorazepam (Ativan).
Which 3 drug classes may be used as anti-epileptics?
- Benzodiazepines.
- Barbituates.
- Anticonvulsants.
Barbituates are CNS _________ and enhance ______, an ________ neurotransmitter.
CNS depressants - enhance GABA, an inhibitory neurotransmitter.
Are benzodiazepines or barbituates more addictive? Which tend to have a higher degree of tolerance?
Barbituates for both.
How can we treat barbituate ODs?
Activated charcoal. Sodium bicarbonate (urinary alkalization).
Barbituates often end in:
-barbital.
List 3 barbituates.
Phenobarbital (Phenobarb).
Pentobarbital.
Secobarbital.
Which benzodiazepine is often abused recreationally?
Alprazolam (Xanax).
Which benzodiazepine is used for roofies?
Flunitrazepam (Rohypnol).
Which barbituate may be used in euthanasia? What else may be used with it?
Secobarbital + antiemetics (ex: metoclopramide).
Which benzodiazepine may be used in euthanasia? What else may be used with it?
Diazepam + paralytic agents (ex: Rocuronium) + anesthesia agents (ex: Propofol).
How do anti-convulsants work?
Alter electrolyte (sodium or calcium) balance to delay action potential and decrease neuronal activity.
Which anti-convulsants decrease sodium cellular influx?
Phenytoin (Dilantin).
Carbamazepine (Tegretol).
Valproic acid (Valproate).
Why do we need to be extra cautious with pheytoin (Dilantin)?
It has a narrow TI and is highly PPB.
List some side effects of anti-convulsants that decrease sodium cellular influx.
Arrhythmias (action potentials altered).
Drug-drug interactions.
Bleeding (d/t vit K interference).
Why might a ketogenic diet be beneficial for seizure control?
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).
What is status epilepticus?
When a seizure of any type progresses to an unstoppable state which becomes life threatening.
Medical emergency!!
What is the first choice of treatment for status epilepticus?
Benzodiazepines (ex: diazepam, lorazepam) IV (NPO d/t respiratory depression).
How do our brains synthesize melatonin?
Pinealocytes in the pineal gland use tryptophan (diet-acquired AA) to make serotonin, which is then converted to melatonin.
Melatonin secretion is regulated via a feedback loop with the:
Hypothalamic SCN.
Do older persons tend to produce more or less melatonin?
Less.
Describe the steps in the onset of sleep.
Circadian rhythm + decreased RAS > decreased cortical stimulation = decreased excitatory neurotransmitter activity (ex: NE, acetylcholine) + increased inhibitory neurotransmitters (serotonin) + increased melatonin synthesis.
What happens to our bodies during REM sleep?
Stage of muscle paralysis, altered VS, decreased BMR & cerebral blood flow; dreaming.
How do the lengths of each sleep stage change as sleep time increases?
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).
What are 5 factors that may increase a pt’s risk for insomnia?
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).
What are the 4 primary types of treatments for insomnia?
Melatonin (synthetic).
Benzodiazepines - Flurazepam (Dalmane), Temazepam (Restoril), Triazolam.
Non-benzodiazepines - namely Buspirone (BuSpar).
Other: antihistamines (ex: diphenhydramine (Benadryl)), antidepressants.
What is the mechanism of action for Buspirone (BuSpar)?
Serotonin agonist (serotonin is an inhibitory, sedative neurotransmitter). Dopamine 2 presynaptic binding (decreases post-synaptic dopamine, which is a precursor to stimulatory catecholamines).
Is it safe to consume CNS depressants with other CNS drugs?
No >:0
Which phase of sleep is obstructive sleep apnea most prevalent in? Why?
REM d/t muscle relaxation.
What is the most prominent risk factor for sleep apnea?
Obesity (increased abdominal pressure > increased thoracic pressure = diaphragm motility decreased).
What are the 3 types of anxiety?
Generalized anxiety.
Panic.
Social phobia.
What are 3 ways to treat anxiety?
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).
