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205 NS - Disease & Pharmacology Flashcards

1
Q

What is the importance of the hippocampus on memory?

A

Consolidation of short-term memory to long-term memory

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2
Q

Which part of the brain is responsible for explicit long-term memory?

A

Hippocampus

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3
Q

Which part of the brain is responsible for skills & habits?

A

Striatum

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4
Q

Which part of the brain is responsible for emotional responses?

A

Amygdala

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5
Q

Which part of the brain is responsible for skeletal musculature?

A

Cerebellum

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6
Q

Why does long-term memory require protein synthesis?

A

To stabilize learning-induced synaptic changes in the brain

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7
Q

Anterograde amnesia

A

Difficulty in acquiring new material & difficulty remembering events since onset of illness/injury

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8
Q

What is the 4AT test?

A

A screening instrument designed for rapid and sensitive initial assessment of cognitive impairment and delirium

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9
Q

What is oxidative stress?

A

Excessive production of reactive oxygen species (ROS), which may form free radicals that are highly reactive and unstable → oxidize other molecules → can result in severe damage & death

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10
Q

What are the therapeutic approaches for stroke?

A

Thrombolytics, neuroprotective agents, preventative

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11
Q

What is the only approved drug for stroke currently?

A

Alteplase (thrombolytics)

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12
Q

What is the MOA of Alteplase?

A

Cause breakdown of the clot by inducing fibrinolysis

activation of plasminogen (inactive) → plasmin (active)

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13
Q

What drugs are used in the prevention of stroke?

A

Blood-thinning agents (Aspirin) & drugs to lower LDL cholesterol (Statins)

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14
Q

Types of drugs to treat Alzheimer’s disease & 1 example of each.

A

Cholinesterase inhibitors - donepezil, rivstigmine, galantamine
NMDA-Receptor Antagonist - memantine

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15
Q

What are the hallmarks of Alzheimer’s disease?

A

Accumulation of beta-amyloid plaques between nerve cells (neurons)

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16
Q

What are the hallmarks of Parkinson’s disease?

A

Histology - the presence of Lewy bodies

Motor - hypokinesia, masked face, lead pipe rigidity, cog-wheel rigidity, resting tremor, shuffling gait

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17
Q

Types of drugs to treat Parkinson’s disease & 1 example of each.

A

Levodopa - in combination with carbidopa & entacapone
Dopamine agonist - pramipexole
MAO-B inhibitors - selegiline
Muscarinic ACh receptor antagonist - orphenadrine

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18
Q

What is the mode of inheritance of Huntington’s disease?

A

Autosomal dominant

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19
Q

What are the hallmarks of Huntington’s disease?

A

Histology - Aggregation of huntingtin protein rich in glutamate repeats
Motor - chorea (dance like movement)

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20
Q

What is the neurobiology of Huntington’s disease?

A
  1. Striatum degenerates → Globus pallidus (GP) less inhibition
  2. GP release more neurotransmitters to the subthalamic nucleus (STN) → higher STN inhibition
  3. Less excitatory neurotransmitter release to Substantia nigra pars reticulata (PR)
  4. PR less excited → reduces inhibitory neurotransmission to the thalamus
  5. Thalamus receives less inhibition from PR → disinhibited → increase transmission from the thalamus to motor cortex → over-stimulation
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21
Q

Types of drugs to treat Huntington’s disease & 1 example of each.

A

Dopaminergic antagonist - tetrabenazine, chlorpromazine, haloperidol

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22
Q

What are the Z-drugs and what are they for?

A

GABA-A receptor agonists

Zolpidem
Zopiclone
Zaleplon

For insomnia

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23
Q

Types of drugs to treat insomnia

Sleep disorders & treatment

A 
Benzodiazepines - GABA-A receptor agonists
Z-drugs - zolpidem, zopiclone, zaleplon
Orexin antagonist - suvorexant
Melatonin agonist - remelteon
Anticonvulsant - gabapentin
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24
Q

Drugs to treat narcolepsy - excessive daytime sleepiness

Sleep disorders & treatment

A

Modafinil

Methylphenidate

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25
Drugs to treat ADHD | Sleep disorders & treatment
Atomoxetine | Adderall - amphetamine
26
Retrograde amnesia
Difficulty in remembering info prior to the onset of illness/injury
27
How's the EEG of partial seizures?
Each has one electrical, usually random & not sync
28
How's the EEG of generalized seizures?
Synchronized activity in all
29
What is status epilepticus?
Continuous or repetitive seizures lasting ≥ 30 mins
30
What are epileptic effectors?
Ion channels & ligand-gated receptors - determine seizure threshold
31
What are epileptic mediators?
Cytokines & prostaglandins - inflammatory mediators, can be therapeutic targets
32
The function of GABA-A receptor
Control the majority of inhibitory signaling in the CNS - controls excessive excitatory effect, puts a cap on it
33
What is the effect of vigabatrin & tiagabin on IPSP?
Prolongs IPSP (↑ half-life of GABA) - ↑ duration
34
What is the effect of barbituates & benzodiazepines on IPSP?
↑ the affinity of GABA for GABA-A receptor - ↑ amplitude
35
What is Generalized Anxiety Disorder (GAD)?
An ongoing state of excessive anxiety lacking any clear reason or focus
36
What are the treatments for Generalized Anxiety Disorder (GAD)?
Cognitive behavioral therapy (CBT) SSRIs/SNRIs Pregabalin Benzodiazepines (short-term)
37
What are the treatments for Panic Disorder?
Cognitive behavioral therapy (CBT) SSRIs/SNRIs Tricyclic antidepressants Benzodiazepines (short-term)
38
What are the treatments for phobias?
Behavioral therapy | SSRIs/SNRIs
39
What are the treatments for Obsessive Compulsive Disorder?
Cognitive behavioral therapy (CBT) SSRIs TCA - Clomipramine
40
How long are benzodiazepines used for?
< 2 weeks
41
What is used for long-term treatment for anxiety disorders?
SSRIs & buspirone
42
MOA of Benzodiazepines
Binds to GABA-A receptors to enhance the action of GABA
43
MOA of SSRIs/SNRIs
Inhibits reuptake of serotonin leading to increased serotonin in the synaptic cleft
44
Inhibitors of monoamine uptake (4)
Selective serotonin (5-HT) reuptake inhibitors (SSRIs) Classic tricyclic antidepressants (TCAs) Newer, mixed 5-HT & noradrenaline reuptake inhibitors Noradrenaline reuptake inhibitors
45
Drug therapy for bipolar disorder
Mood stabilizers - lithium & certain anticonvulsants: valproate, carbamazepine 2nd-gen antipsychotics: aripiprazole, quetiapine, risperidone
46
Name a 1st-gen & 2nd-gen antipsychotic drug.
1st-gen: Chlorpromazine | 2nd-gen: Clozapine
47
What are the 4 characteristic symptoms of the neuroleptic malignant syndrome in order?
Altered mental status Motor abnormalities Hyperthermia Autonomic hyperactivity
48
What may cause neuroleptic malignant syndrome?
Antipsychotics - haloperidol, olanzapine Antiemetics - metoclopramide Withdrawal of antiparkinson drugs
49
What's the management of neuroleptic malignant syndrome?
Rapid cooling Benzodiazepines Dantrolene Bromocriptine/amantadine
50
Where do primary brain tumors originate from?
In the brain either in brain parenchyma or extraneural structures
51
Where do secondary brain tumors (brain metastases) originate from?
Originate in tissues outside the brain & spread to the brain
52
Are primary or secondary brain tumors more common?
Secondary brain tumors (brain metastases) are ~10x more common
53
Drugs approved for brain tumors. (6)
``` Bevacizumab Carmustine Everolimus Lomustine Naxitamab-gqgk Temozolomide ```
54
"All-or-none" principle
Action potential, not graded | Constant amplitude
55
Action potential mechanism
1. Hypopolarization 2. Depolarization 3. Overshoot 4. Repolarization 4. Hyperpolarization.
56
Refractory period
Period during an action potential when no further excitation can occur
57
Which domain of the voltage-gated sodium channel contains the voltage sensor?
4th TM domain - when sense change in voltage, it moves up changing the conformation → channels open
58
Conformational states of voltage-gated sodium channel
Deactivated → open → inactivated → repolarization
59
Deactivated state of voltage-gated sodium channel
Channels are deactivated | M-gate is closed, doesn't let Na+ through
60
Activated state of voltage-gated sodium channel
Current passes through and changes voltage difference across membrane Channel activates → m-gate open
61
Inactivated state of voltage-gated sodium channel
Neuron depolarizes | H-gate swings shut and blocks Na+ from entering cell
62
Passive signals (Graded potential)
Diminish as they spread from their site of initiation
63
Strategies to increase current spread along axon
Increase axon diameter | Reduce membrane current leak - adding insulating material
64
3 morphological type of synapses
Axodendritic (very common) Axosomatic (common) Axoaxonic (uncommon)
65
Depolarising influences
Positive charges moving in | Negative charges moving out
66
Hyperpolarising influences
Positive charges moving out | Negative charges moving in
67
Ionotropic receptors vs Metabotropic receptors
Ionotropic - direct gating | Metabotropic receptors - indirect gating
68
Local anesthetics
Analgesia close to source of pain
69
Central analgesia
Analgesia through central/spinal sites w/o loss of consciousness
70
General anesthesia
Loss of consciousness ± analgesia
71
Opium alkaloids
Morphine
72
Metabolism of opiod analgesics
Phase 1 metabolism: CYP pathway Phase 2 conjugation - can be both
73
Why do drugs have to be metabolized?
So they can: 1. Be excreted 2. Reach their target site
74
β-arrestin recruitment is involved in:
Internalization & recycling of opioid receptors | Recruit further signaling molecules to modify neuronal function
75
Opioid receptor signaling
1. Opioid agonist G-protein activation 2. Receptor phosphorylation 3a. Arrestin recruitment 3b. Internalization 4. MAPK signaling 5. Recycling
76
Endogenous opioids
Endorphins | Enkephalins
77
Analgesic tolerance
A gradual decrease in analgesic efficacy over time | Requirement of escalation in opioid dose to maintain analgesia
78
Where are opioid receptors found?
On presynaptic terminal of primary afferent nociceptors & 2° neurons
79
RAVE hypothesis
Endocytosis resensitizes receptors - Receptor Activation Versus Endocytosis Strong recycling → no tolerance No recycling → tolerance
80
Paracetemol (acetaminophen) | analgesics
Analgesic & antipyretic
81
Aspirin | analgesics
Anti-platelet Anti-inflammtory Should not be used in age <16 y.o.
82
NSAIDs | analgesics
Ibuprofen Reduce inflammation, analgesics, antipyretic
83
Opioid analgesics | analgesics
Morphine - full agonist at μ-opiod receptor | Codeine - partial μ-receptor agonist
84
First-line treatment of neuralgic pain treatment | analgesics
Anticonsulvants - gabapentin, pregabalin
85
Migraine treatments | analgesics
Triptans (Serotonin 5HT1 Receptor Agonists) - Sumatriptan
86
COX-2
Enzyme responsible for inflammation and pain
87
Meningitis
Infection & inflammation of the meninges Pyogenic - bacterial Aseptic - viral
88
Pyogenic meningitis pathology?
Thick layer of exudate | Neutrophils
89
How do pathogens reach meninges?
``` Haematogenous spread Adjacent infections Neurosurgery Trauma Remote foci of infection ```
90
Cause of acute bacterial meningitis
Streptococcus pneumoniae
91
Causes of viral meningitis
Enteroviruses - coxsackie virus | HSV-2
92
Risk factors of bacterial meningitis
Decreased cell-mediated immunity Neurosurgery/head trauma Fracture of cribiform plate
93
What's the most common viral cause of chronic meningitis?
HIV
94
Distinguishing feature of Neisseria meningitis
Petechial rash can rapidly become purpuric
95
3 main considerations of empirical antimicrobials for bacterial meninges
1. Must cross BBB 2. Bactericidal 3. Active against most common pathogens
96
Encephalitis
Inflammation of brain
97
Causes of encephalitis
Viruses
98
Treatment for HSV & Varicella-Zoster virus
Acyclovir
99
Treatment for cytomegalovirus
Ganciclovir
100
Encephalopathy
Altered brain function w/o inflammation, mostly non-infectious 腦病
101
Brain abscess
Intracerebral infection, collection of pus
102
Do virus cause brain abscesses?
No
103
Subdural empyema
Collection of pus between dura & arachnoid matter layer of meninges
104
Epidural empyema
Between dura matter and skull/vertebral column
105
Key diff between empyema & other brain infections
No need to cross BBB to cause disease
106
Acute flaccid myelitis
Infection of the spinal cord
107
Brain barriers to infection
Physical protection - skull/vertebrae, meninges, CSF Brain-CSF barrier BBB Olfactory portal
108
Mechanism of bacterial invasion of blood-brain & blood-CSF barriers
Transcellular penetration Paracellular entry "Trojan horse" mechanism
109
What protects the brain from infection?
Nasal cavity harbor normal bacterial flora Cells secrete mucins Mucocilliary process Secretion of antimicrobial substances Tight junctions between epithelial cells DC extend processes into nasal cavity to help macrophages clear foreign antigens
110
Treatment of trigeminal neuralgia | analgesics
Carbamazepine
111
MOA of antipsychotics
Inhibit dopamine D2 receptors

MBBS (28 decks)

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