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201 cns Flashcards

1
Q

What is epilepsy?

A

-sudden excessive high frequency neuronal discharge
-highly synchronous discharges (not random)
-may be loss of consciousness
-behavioral changes related to sire of discharge.

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2
Q

risk factors of sezuires

A

-disturbed water/electrolyte levels
-disturbed glucose levels
-raised body temperature
-sleep disturbance
-toxicity
-heredity
-tumors

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3
Q

diagnosis of epilepsy

A

-seizures must be recurrent and spontaneous
-EEG records abnormal electrical charges

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4
Q

types of generalized seizures

A
  • tonic-clonic seizures ( patient falls, stiffens, convulses, hyper-salivation, laboured breathing)
  • tonic (stiffening of body)
  • clonic (impairment of consciousness)
    -absence ( eyelids flutter, head drops)
    -myoclonic ( involuntary,s shock-like jerks)
    -atonic (sudden loss of muscle tone)
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5
Q

types of focal seizures

A

-simple focal ( retains awareness)
-complex focal ( altered awareness, confusion)
-secondarily generalized seizures ( focal seizure that lead to tonic-clonic seizure)

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6
Q

what is status epilepticus ?

A

tonic-clonic seizure lasts more than 5 minutes, person doesn’t regain consciousness in between

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7
Q

how do seizures arise?

A

dynamic between excitation and inhibition is disturbed ( loss of inhibition)

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8
Q

how do seizures stop without intervention?

A
  • K channel activation
    -Na channel deactivation
  • glutamate receptor desensitization
  • glutamate depletion
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9
Q

how do antiepileptics work?

A
  • decrease excitatory mechanism
  • inhibit glutamate neurotransmission
  • inhibition of calcium channel
    -enhancement of GABA function
  • inhibition sodium channels ( preferentially block cell that are firing repetitively, not all of them)- prefer the inactivated state of sodium channels, preventing them from becoming activated)
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10
Q

Drugs that reduce glutamate release

A

-lamotrigine, phenytoin, carbamazepine, sodium valproate ( Na- channel block)
-gabapentin, pregabalin ( Ca- channel block)
-levetiracetam (reducing vesicle fusion)

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11
Q

Drugs acting at GABA synapses

A
  • vigabatrin, sodium valproate (increase GABA levels)
    -tiagabine ( decrease GABA inactivation)
    -benzodiazepines ( prolong channels open time)
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12
Q

Non- pharmacological treatment of epilepsy

A
  • surgery
    -vagus nerve stimulation (stimulation with a pacemaker type device)
    -deep brain stimulation
    -ketogenic diet ( brain is forces to use ketones rather than glucose)
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13
Q

sodium valproate (indication, monitoring, precautions)

A

-can be used for all forms of epilepsy
-monitor liver function before therapy and during first months
-measure full blood count and ensure no undue potential bleeding before starting
-highly teratogenic ( contraception needed)
-vitamin D supplementation

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14
Q

carbamazepine (indication, monitoring, precautions)

A

-focal and secondary generalized tonic-clonic
-primary generalized tonic-clonic
-monitor plasma concentration for optimum response 4-12 mg/L measured after 1-2 weeks
-blood counts and hepatic and renal function test
-increased risk of stevens-jonson syndrome
-vitamin D supplementation

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15
Q

lamotrigine (indications, monitoring, precautions)

A
  • used for monotherapy of focal, primary and secondary generalized tonic-clonic or seizures associated with Lennox-Gastaut syndrome
  • plasma drug concentration should be monitored before, during and after pregnancy
    -can cause hypersensitivity (skin rash)
    -can cause bone marrow failure
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16
Q

levetiracetam (indications, monitoring, precautions )

A

-used for monotherapy of focal seizures
-monitor plasma concentrations during pregnancy
-can cause depressions and suicidal ideation emerge
-increased risk of somnolence or other CNS side effects

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17
Q

what are the symptoms of Parkinson’s disease?

A

Cardinal: -tremor
-bradykinesia
-rigidity
-postural instability
Other symptoms: mental changes,
constipation, sexual dysfunction, urinary problems, sleep disturbances, pain, impulsive behavior

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18
Q

what is the pathology of Parkinson’s disease?

A
  • lewy bodies (contain alpha-synuclein)
  • aggregated of alpha- synuclein
    -leading pathogenic hallmarks in brain biopsies
    -loss of DA producing neurons in substantia nigra- imbalance in direct and indirect pathways
    -loss of cotrico-spinal output
    -decreased movement, rigidity
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19
Q

what are treatment options for parkinson

A

-L- dopa: replace dopamine
-AADC inhibitors: increase availability
- MAO-B inhibitors: decrease breakdown eg. entacapone, rasagiline, selegiline
- D2 agonists: rotigotine (patch), apomorphine (in advanced PD)
-glutamate antagonists (amantadine) reduce dyskinesia cause by levodopa

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20
Q

Levadopa therapy

A
  • levadopa is given with cabidopa (inhibit dopa decarboxylase) to enable it to cross BBB and prevent breakdown in the gut
    -long term use can cause dyskinesia and motor fluctuations
    -Late and missed doses can lead to complications such as pneumonia and falls
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21
Q

what are the risk factors of PD?

A
  • increasing age
    -male
  • head trauma
    -genetic mutation
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22
Q

treatment for Alzheimer’s disease

A

-acetylcholinesterase inhibitors (increases acetylcholine)
(donepezil, galantamine, rivastigmine)
-NMDA receptor antagonists (memantine)
(reduces glutamate because it creates oxidative stress which breaks down proteins and nucleic acid so it contributes to cell death)
-new drug: lecanemab (reduce αβ)

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23
Q

what are the symptoms of dementia

A

cognitive: memory loss, lack of concetration, disorientated, speech difficulties
non-cognitive: agitation, aggression, distress, psychosis

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24
Q

diagnosis for dementia

A

-Alzheimer’s: >60, memory loss
-vascular: screened for depression, psychomotor retardation
-lewy body: visual hallucinations and parkinson symptoms
-frontotemporal: <65, semantic, non-fluent

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25
Q

what are the symptoms of schizophrenia and what are the pathways associated with them

A

-positive: hallucinations, delusions (mesolimbic pathway)
-negative: emotional apathy, social withdrawal (mesocortical pathway)
-cognitive: disturbance of normal thought processes

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26
Q

first vs second generation antipsychotic drugs

A

-first: block D2 receptors, more likely to cause side effects eg. phenothiazine derivatives, haloperidol
-second: act on a range of receptors, lower risk of extrapyramidal symptoms and dyskinesia but associated with weight gain and glucose intolerance eg. aripiprazole, clozapine, olanzapine

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27
Q

what are common side effects of antipsychotics

A

-hyperprolactinaemia (risperidone, amisulpride, sulpiride and 1st gen.)
-sexual dysfunction (risperidone, haloperidol, olandapine)
-CVS (primozide)
-hypotension (clozapine, quetiapine)
-weight gain (clozapine, olazapine)
-hyperglycemia and diabetes
-NMS (all of them)- requires weekly monitoring first 6 weeks then 12 weeks then 1 year.(weight, glucose, lipid, ECG, blood pressure, blood test, liver function)

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28
Q

what are the requirements for high dose antipsychotics

A
  • initial prescription should be written as single dose until effects have been reviewed
    -oral and intramuscular dugs should be proscribed separately
    -patient should be monitored every 15 minutes
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29
Q

structural deficit of schizophrenia

A

-disruption of neuronal migration
-enlarged ventricles
-reduced regional cerebral volumes
-loss of neurons
-biomarkers in EEG: changes in response to external stimuli

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30
Q

mechanism of typical (first gen.) psychotics

A

high affinity D2 receptor antagonists (phenothiazines, haloperidol)
effective only against positive symptoms
serious side effect: DA-related: pseudoparkinsonism, tardive dyskinesia, akathisia, sexual dysfunction
non-DA: sedation, hypotension, peripheral autonomic

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31
Q

mechanism of atypical (second gen.) psychotics

A

low affinity for D2 receptors
benzamides
less side effects
can cause weight gain and diabetes

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32
Q

what is drug tolerance

A

-desensitization of receptors, higher doses are required to achieve the effect
-β-arrestin prevent G proteins subunits coupling and block the receptor. this limits the receptor availability for agonist binding

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33
Q

what is withdrawal syndrome

A

-insomnia, anxiety, loss of appetite, weight loss, tremor
-long-acting benzodiazepines: symptoms develop withing 3 weeks
-short-acting benzodiazepines: develop in a day

34
Q

classify mood disorders

A

-bipolar: type I, ii , cyclothemia (mood swings from mania to depression)
-unipolar: major depression, dysthimic depression

35
Q

what are the two types of depression

A

-reactive depression: non-familial, associated with stressful event, temporary
-endogenous depression: familial, not related to external stressors, chronic

36
Q

what are the symptoms of depression

A

misery, apathy, suicidal thoughts, loss of self-esteem
biological: weight loss, loss of libido, sleep disturbances

37
Q

what are the causes of mood disorders

A

-genetic-hereditary (bipolar)
-environmental factors (stressful event)
-neurotransmitter dysfunction (monoamine)
*catecholamines: dopamine, NA, adrenaline
indolamines: serotonin

38
Q

how do we treat depression

A

monoamine oxidase B inhibitors (interaction with food rich in tyramine) eg. selegiline s/e: postural hypotension
tricyclic antidepressants: block reuptake of serotonin and norepinephrine eg. amitriptyline (side-effects: sedation, postural hypotension, mania, convulsions, heart block, dangerous in overdose- respiratory depression, arrythmia, coma, long half-lives)
SSRIs: block reuptake of serotonin (safer, more efficient)
eg. sertaline (safer in patients with unstable angina or recent myocardial infraction) s/e: nausea, tremor, tachycardia, convulsions,
can cause withdrawal (GI and sleep disturbances, anxiety, dizziness, fatigue, sweating)
risk of serotonin syndrome (tremor, rigidity, tachycardia, BP, shivering, diarrhea, confusion, mania)
atypical: mirtazapine (H antagonism)

39
Q

how do we treat bipolar disorders

A

-lithium: can reduce both mania and depression
(can cause lithium toxicity- needs plasma monitoring 0.4-1 mmol/l)
-anticonvulsants: reduce excitability eg. carbamazepine, valproate, lamotrigine
-atypical: olanzapine, risperidone, aripiprazole

40
Q

how do we assess depression

A
  • one key symptom(persistent sadness, marked loss of interest)
    -if present, ask about associated symptoms
    (sleep disturbance, loss of appetite, suicidal thoughts, poor concertation, slow movements)
41
Q

what are side-effects of antidepressants

A

Serotonin syndrome: tremors, rigidity, tachycardia, hypertension, diarrhea, confusion)
-suicidal behaviour
-discontinuation syndrome: anxiety, headache, dizziness, GI (occur within 5 days)

42
Q

what is the treatment of nausea

A

-motion sickness: hyoscine bromide
-chemotherapy: prochlorperazine
-underlying conditions: cinnarizine
-GI disease: metoclopramide
-palliative care: haloperidol, levomepromazine
-metoclopramide: stimulates gastric emptying (can cause dystonia in young females)
-domperidone: act at the chemoreceptor trigger zone
(can cause arrythmia)
-phenothiazines: block the chemoreceptor trigger zone

43
Q

what is the nausea treatment in pregnancy

A

-self-care advice (rest, or hydration and dietary changes)
-antiemetics (chlorpromazine, cyclizine, metoclopramide)
-in persistent hyperemesis gravidarum: offer parietal or rectal antiemetics + thiamine supplements to reduce the risk of Wernicke’s encephalopathy

44
Q

what should you do before starting adhd treatment?

A

-confirm the diagnosis of adhd
-review of mental health comorbidities
-risk assessment for substance misuse
-review physical health (weight, height, BP, pulse)

45
Q

what is treatment for adhd?

A

-lisdexamphetamine or methylphenidate (dopamine and norephedrine reuptake inhibitor- stimulant)- increase cognitive function, reduce hyperactivity and distractibility
(stimulants can cause high HR and BP, insomnia, loss of appetite, vomiting, abdo pain, less growth)
-if poor response or tolerance, give atomoxetine (inhibits noradrenaline reuptake- non-stimulant)

46
Q

how does methylphenidate (psychostimulant) work in adhd

A

-it increases levels of dopamine and norepinephrine by blocking their reuptake

47
Q

what is happening to the brain and body when it’s anxious

A

-individuals with anxiety disorder have higher activity in limbic system
-amygdala initiate the flight-fight response
-increase noradrenergic pathway
-suppress serotonergic pathway
-brain releases ACTH which triggers the release of cortisol from the adrenal gland

48
Q

what are the different types of anxiolytics

A

-adrenergic β-receptor blockers (beta blockers)
(manage sympathetic activity, treat symptoms)
-serotonergic agonist:
buspirone: serotonin agonist
SSRIs: serotonin reuptake inhibitors
venflaxine: noradrenaline and 5HT uptake blockers
-GABAergic pathways: target GABA ligand gated channel
diazepam: increases frequency of channel opening (hyperpolarisation=inhibitory)- can cause respiratory depression and withdrawal syndrome (reduce dose by 1-2mg every 1-2 weeks)

49
Q

what are the functions of sleep

A

-restorative
-adaptation (protection from nocturnal predators)
-energy conservation
-memory consolidation and integration

50
Q

what are the two different types of sleep

A

-REM: associated with dreaming (small waves, high frequency)
(20-10 minutes) -occasional involuntary movement
-Non-REM: deep sleep, 4 stages (slow waves, large amplitude)
(60-90 minutes)- muscle paralysis

51
Q

what is the sleep cycle

A

-periods of REM and non-REM
-each cycle has shorter and shallower non-REM and longer REM periods

52
Q

what is the RAS -thalamus-cortical interaction

A

-when awake, RAS activates thalamus which generates non-rhythmic activity-cortex entrained into fast waking activity
-when asleep, RAS activity is switched off, thalamus generates rhythmic activity, cortex entrained into slow sleep rhythms

53
Q

what can cause chronic insomnia?

A

-pain, depression, alcohol abuse, breathing problems

54
Q

what is the treatment of insomnia

A

-benzodiazepines (decrease time taken to fall asleep)
short-acting (<8 hrs) :loprazolam, temazepam (less hangover effect)
long-acting (>20 hrs) : diazepam, nitrazepam
problems with tolerance, dependence and rebound insomnia
-zolpidem, zoplicone:
bind in similar wan as BZD (bind to alpha 1 subtypes_more sedative effect, less anxiolytic effect)
-melatonin, ramelton: hormone that promotes sleep initiation and resets ricadian clock
-histamine H1 antagonists
-orexin antagonists (suvorexant)

55
Q

what are the three types of blood-brain barrier

A

-blood-brain barrier
-blood-csf barrier
-the arachnoid barrier

56
Q

how does the blood-brain barrier protect the brain

A

-tight junctions
-absence of fenestrations
-active transport mechanism
-drug metabolizing enzymes in brain endothelial cells

57
Q

which drugs can cross the bool-brain barrier by passive diffusion

A

-lipid-soluble molecules
-low polar surface area
-low molecular weight

58
Q

how do drugs cross the blood-brain barrier

A

-passive diffusion
-active transport (xenobiotics, metabolites, toxins,drugs)
-carrier-mediated transport (glucose, amino acid)-donepezil
-transcytosis:
receptor-mediated(proteins, hormones, growth factors)
adsorptive-mediated(positively charged, large molecules, histone, protamine, cationic proteins)
-cell diapedesis (WBC): able to cross the endothelial BBB

59
Q

what is the lipinksi’s rule of 5?

A

-5 or fewer hydrogen bond donors
-10 or fewer hydrogen bond acceptors
-molecular weight under 500g/ml
-LogP less than 5
-10 or fewer rotatable bonds

60
Q

what are the chemical methods to improve the physiochemical properties of dugs?

A

-make them more lipophilic by adding lipid groups to polar ends of drug molecules (can lead to poor tissue distribution, change bioavailability)
-prodrugs (drugs must undergo chemical conversion before becoming active)- alter the tissue distribution, efficacy, toxicity
-chemical delivery systems (enzymatic physiochemical, site-specific enzyme activated, receptor-based)
two types of bioremovable moieties: targetor (responsible for site-specificity), modifier (lipophilizer, protect certain functions, prevent unwanted or premature metabolic conversions)
-molecular packaging (increase lipophilicity, prevent premature degradation, make targeting possible)

61
Q

why is L-Dopa given with carbidopa or benserazide?

A

-inhibit DOPA decarboxylase
-minimize peripheral degradation

62
Q

how do donepezil, methylphenidate l-dopa cross the BBB?

A

-donepezil: transported by an organic cation transporter
-methylphenidate: by passive diffusion
-L-dopa: carrier transport

63
Q

what are the stages of analgesia

A

1.Analgesia: conscious, drowsy, amnesia
2.excitment: loss of consciousness, irregular cardio reparation,
apnea, spasticity, vomiting
3.anaesthisia: regular respiration, loss of reflux and muscle tone
4.meduallry paralysis: depression of cardiorespiratory and death

64
Q

what are the types of anesthesia

A

-systemic
-regional
-local

65
Q

how do inhalation anaesthetics work?

A

-gases or vapors administered via vaporizers
-controllable, rapid blood-gas exchange
-eg, osioflurane: cause coronary problems, not safe in malignant hyperthermia, fluorine produced can cause renal impairment
>sevoflurane< (potent, hepatotoxic)
-measure the MAC using the oil/gas partition coefficient
-the one with the lower MAC is more potent
-potency is proportional to lipid solubility
-anesthetics interact with membrane proteins (receptors and ligand-gated ion channels)

66
Q

how do thiopetal, propofol and etomidate (IV) anesthetics work?

A
  • Thiopetal: positive allosteric modulator of GABA (barbiturate binding site)
    -increase the frequency of channel opening
    -can cause porphyria, respiratory depression, myocardial depression, bronchospasm
    -Propofol: binds to alcohol binding site (increase frequency of GABA channel opening)
    -etomidate: bind to GAs binding site (respiratory depression, porphyria)
67
Q

how does ketamine (IV) anesthetic work?

A

-competitively antagonise glutamic acid-mediated NMDA activation (blocks sodium and calcium, no AP)
-can also interact with opioid receptors and muscarinic
-works as an analgesic
-can cause high HR, BP, RR, high muscle movement , hallucinations and nightmares

68
Q

what are the side effects of clozapine

A

-agranulocytosis
-intestinal obstruction
-cardiomyopathy
higher risk when: patient stops smocking or switches to e cigarrete, takes concomitant medicines, has pneumonia, has reduced clozapine metabolism or suspected toxicity

69
Q

what are the main information of lithium

A
  • therapeutic levels :0.4-1 mmol/litre
    -carer advice: report signs of lithium toxicity, hypothyroidism, renal dysfuction, drink fluids and avoid dietary changes that cause sodium disturbances, avoid alcohol cause it causes drowsiness, carry lithium card alert
    -monitoring: full blood count, BMI, serum electrolytes, ECG
    -long term use effects: teratogenic, low seizure threshold, QT prolongation, renal impairment, thyroid disorders
    -sign of toxicity: GI disturbances, renal impairment, visual disturbances, arrythmias, CNS disturbances, EPS
70
Q

what are the types of headaches

A

-primary headache: not associated with underlying conditon
-secondary: associated with underlying condition

71
Q

how do you assess headaches

A

-pain (onset, duration, frequency, location, severity)
-associated symptoms: aura, nausea, photophobia, phonophobia
-associated with a trigger
-medication used and if it worked
-vital signs, mental state, alertness, neuro exam

72
Q

what are the types of migraine

A

-episodic (<15 days a month)
-chronic (>15 days a month)
-migraine without aura (with nausea, photophobia, phonophobia)
-migraine with aura (visual, sensory or speech)
-atypical aura (motor weakness, double vision, visual symptoms in one eye, poor balance, reduced consciousness)

73
Q

what are the triggers for migraine

A

-poor sleep
-stress
-menstruation
-excess caffeine
-missed meals

74
Q

what is the management of migraine

A

-analgesics (paracetamol, aspirin, NSAID)
-anti-emetics (prochlorperazine, metoclopramide)
-triptans (sumatriptans-preferred in pregnancy)
5-HT1 receptor agonists ( cranial vessel vasodilation)
-if ineffective: alternative triptan or combine with analgesic
-refer

75
Q

what is the prophylactic treatment

A

-propranolol
-topiramate (teratogenic)
-amitriptyline

76
Q

what is cluster headache

A
  • severe pain lasting from 15 minutes - 3 hours
    At least 1:
    -eyelid swelling
    -nasal congestion
    -facial flushing/sweating
    -fullness in ear
77
Q

what is the management of cluster headache

A

-triptan (over 18s)
-oxygen therapy
-prophylactic: verapamil

78
Q

what are the two intraspinal routes

A

-epidural: administer anesthetics into the epidural space for regional pain relief
-intrathecal: administer in the CSF for pain relief but also for antibiotics or cytoxins (max 10mL)

79
Q

what are the formulation requirements for intrathecal formulations

A

-sterile, pyrogenic-free, isosmotic with CSF
-preservative-free

80
Q

what are polymer implants for brain delivery

A

-carmustine: drug for malignant tumor (severe side effects)
-can be administered directly to brain (less side effects)
-using polymer implants (made of co-polymer using (carboxyphenoxy)-propane and sebacic acid)
-consitsts of hydrophobic outer layer which prevents water ingress to the deeper layers therefore protecting the drug)
-up to 8 gliadel wafers can be inserted at the resection site
*anhydride too reactive, ester take too long

201 cns (9 decks)

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