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MBBS > 205 NS - Disease & Pharmacology > Flashcards

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
Q

Drugs to treat ADHD

Sleep disorders & treatment

A

Atomoxetine

Adderall - amphetamine

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26
Q

Retrograde amnesia

A

Difficulty in remembering info prior to the onset of illness/injury

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27
Q

How’s the EEG of partial seizures?

A

Each has one electrical, usually random & not sync

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28
Q

How’s the EEG of generalized seizures?

A

Synchronized activity in all

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29
Q

What is status epilepticus?

A

Continuous or repetitive seizures lasting ≥ 30 mins

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30
Q

What are epileptic effectors?

A

Ion channels & ligand-gated receptors - determine seizure threshold

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31
Q

What are epileptic mediators?

A

Cytokines & prostaglandins - inflammatory mediators, can be therapeutic targets

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32
Q

The function of GABA-A receptor

A

Control the majority of inhibitory signaling in the CNS - controls excessive excitatory effect, puts a cap on it

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33
Q

What is the effect of vigabatrin & tiagabin on IPSP?

A

Prolongs IPSP (↑ half-life of GABA) - ↑ duration

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34
Q

What is the effect of barbituates & benzodiazepines on IPSP?

A

↑ the affinity of GABA for GABA-A receptor - ↑ amplitude

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35
Q

What is Generalized Anxiety Disorder (GAD)?

A

An ongoing state of excessive anxiety lacking any clear reason or focus

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36
Q

What are the treatments for Generalized Anxiety Disorder (GAD)?

A

Cognitive behavioral therapy (CBT)
SSRIs/SNRIs
Pregabalin
Benzodiazepines (short-term)

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37
Q

What are the treatments for Panic Disorder?

A

Cognitive behavioral therapy (CBT)
SSRIs/SNRIs
Tricyclic antidepressants
Benzodiazepines (short-term)

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38
Q

What are the treatments for phobias?

A

Behavioral therapy

SSRIs/SNRIs

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39
Q

What are the treatments for Obsessive Compulsive Disorder?

A

Cognitive behavioral therapy (CBT)
SSRIs
TCA - Clomipramine

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40
Q

How long are benzodiazepines used for?

A

< 2 weeks

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41
Q

What is used for long-term treatment for anxiety disorders?

A

SSRIs & buspirone

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42
Q

MOA of Benzodiazepines

A

Binds to GABA-A receptors to enhance the action of GABA

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43
Q

MOA of SSRIs/SNRIs

A

Inhibits reuptake of serotonin leading to increased serotonin in the synaptic cleft

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44
Q

Inhibitors of monoamine uptake (4)

A

Selective serotonin (5-HT) reuptake inhibitors (SSRIs)
Classic tricyclic antidepressants (TCAs)
Newer, mixed 5-HT & noradrenaline reuptake inhibitors
Noradrenaline reuptake inhibitors

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45
Q

Drug therapy for bipolar disorder

A

Mood stabilizers - lithium & certain anticonvulsants: valproate, carbamazepine
2nd-gen antipsychotics: aripiprazole, quetiapine, risperidone

46
Q

Name a 1st-gen & 2nd-gen antipsychotic drug.

A

1st-gen: Chlorpromazine

2nd-gen: Clozapine

47
Q

What are the 4 characteristic symptoms of the neuroleptic malignant syndrome in order?

A

Altered mental status
Motor abnormalities
Hyperthermia
Autonomic hyperactivity

48
Q

What may cause neuroleptic malignant syndrome?

A

Antipsychotics - haloperidol, olanzapine
Antiemetics - metoclopramide
Withdrawal of antiparkinson drugs

49
Q

What’s the management of neuroleptic malignant syndrome?

A

Rapid cooling
Benzodiazepines
Dantrolene
Bromocriptine/amantadine

50
Q

Where do primary brain tumors originate from?

A

In the brain either in brain parenchyma or extraneural structures

51
Q

Where do secondary brain tumors (brain metastases) originate from?

A

Originate in tissues outside the brain & spread to the brain

52
Q

Are primary or secondary brain tumors more common?

A

Secondary brain tumors (brain metastases) are ~10x more common

53
Q

Drugs approved for brain tumors. (6)

A 
Bevacizumab
Carmustine
Everolimus
Lomustine
Naxitamab-gqgk
Temozolomide
54
Q

“All-or-none” principle

A

Action potential, not graded

Constant amplitude

55
Q

Action potential mechanism

A
  1. Hypopolarization
  2. Depolarization
  3. Overshoot
  4. Repolarization
  5. Hyperpolarization.
56
Q

Refractory period

A

Period during an action potential when no further excitation can occur

57
Q

Which domain of the voltage-gated sodium channel contains the voltage sensor?

A

4th TM domain

  • when sense change in voltage, it moves up changing the conformation → channels open
58
Q

Conformational states of voltage-gated sodium channel

A

Deactivated → open → inactivated → repolarization

59
Q

Deactivated state of voltage-gated sodium channel

A

Channels are deactivated

M-gate is closed, doesn’t let Na+ through

60
Q

Activated state of voltage-gated sodium channel

A

Current passes through and changes voltage difference across membrane
Channel activates → m-gate open

61
Q

Inactivated state of voltage-gated sodium channel

A

Neuron depolarizes

H-gate swings shut and blocks Na+ from entering cell

62
Q

Passive signals (Graded potential)

A

Diminish as they spread from their site of initiation

63
Q

Strategies to increase current spread along axon

A

Increase axon diameter

Reduce membrane current leak - adding insulating material

64
Q

3 morphological type of synapses

A

Axodendritic (very common)
Axosomatic (common)
Axoaxonic (uncommon)

65
Q

Depolarising influences

A

Positive charges moving in

Negative charges moving out

66
Q

Hyperpolarising influences

A

Positive charges moving out

Negative charges moving in

67
Q

Ionotropic receptors vs Metabotropic receptors

A

Ionotropic - direct gating

Metabotropic receptors - indirect gating

68
Q

Local anesthetics

A

Analgesia close to source of pain

69
Q

Central analgesia

A

Analgesia through central/spinal sites w/o loss of consciousness

70
Q

General anesthesia

A

Loss of consciousness ± analgesia

71
Q

Opium alkaloids

A

Morphine

72
Q

Metabolism of opiod analgesics

A

Phase 1 metabolism: CYP pathway
Phase 2 conjugation

  • can be both
73
Q

Why do drugs have to be metabolized?

A

So they can:

  1. Be excreted
  2. Reach their target site
74
Q

β-arrestin recruitment is involved in:

A

Internalization & recycling of opioid receptors

Recruit further signaling molecules to modify neuronal function

75
Q

Opioid receptor signaling

A
  1. Opioid agonist G-protein activation
  2. Receptor phosphorylation
    3a. Arrestin recruitment
    3b. Internalization
  3. MAPK signaling
  4. Recycling
76
Q

Endogenous opioids

A

Endorphins

Enkephalins

77
Q

Analgesic tolerance

A

A gradual decrease in analgesic efficacy over time

Requirement of escalation in opioid dose to maintain analgesia

78
Q

Where are opioid receptors found?

A

On presynaptic terminal of primary afferent nociceptors & 2° neurons

79
Q

RAVE hypothesis

A

Endocytosis resensitizes receptors - Receptor Activation Versus Endocytosis

Strong recycling → no tolerance
No recycling → tolerance

80
Q

Paracetemol (acetaminophen)

analgesics

A

Analgesic & antipyretic

81
Q

Aspirin

analgesics

A

Anti-platelet
Anti-inflammtory

Should not be used in age <16 y.o.

82
Q

NSAIDs

analgesics

A

Ibuprofen

Reduce inflammation, analgesics, antipyretic

83
Q

Opioid analgesics

analgesics

A

Morphine - full agonist at μ-opiod receptor

Codeine - partial μ-receptor agonist

84
Q

First-line treatment of neuralgic pain treatment

analgesics

A

Anticonsulvants - gabapentin, pregabalin

85
Q

Migraine treatments

analgesics

A

Triptans (Serotonin 5HT1 Receptor Agonists) - Sumatriptan

86
Q

COX-2

A

Enzyme responsible for inflammation and pain

87
Q

Meningitis

A

Infection & inflammation of the meninges

Pyogenic - bacterial
Aseptic - viral

88
Q

Pyogenic meningitis pathology?

A

Thick layer of exudate

Neutrophils

89
Q

How do pathogens reach meninges?

A 
Haematogenous spread
Adjacent infections
Neurosurgery
Trauma
Remote foci of infection
90
Q

Cause of acute bacterial meningitis

A

Streptococcus pneumoniae

91
Q

Causes of viral meningitis

A

Enteroviruses - coxsackie virus

HSV-2

92
Q

Risk factors of bacterial meningitis

A

Decreased cell-mediated immunity
Neurosurgery/head trauma
Fracture of cribiform plate

93
Q

What’s the most common viral cause of chronic meningitis?

A

HIV

94
Q

Distinguishing feature of Neisseria meningitis

A

Petechial rash can rapidly become purpuric

95
Q

3 main considerations of empirical antimicrobials for bacterial meninges

A
  1. Must cross BBB
  2. Bactericidal
  3. Active against most common pathogens
96
Q

Encephalitis

A

Inflammation of brain

97
Q

Causes of encephalitis

A

Viruses

98
Q

Treatment for HSV & Varicella-Zoster virus

A

Acyclovir

99
Q

Treatment for cytomegalovirus

A

Ganciclovir

100
Q

Encephalopathy

A

Altered brain function w/o inflammation, mostly non-infectious

腦病

101
Q

Brain abscess

A

Intracerebral infection, collection of pus

102
Q

Do virus cause brain abscesses?

A

No

103
Q

Subdural empyema

A

Collection of pus between dura & arachnoid matter layer of meninges

104
Q

Epidural empyema

A

Between dura matter and skull/vertebral column

105
Q

Key diff between empyema & other brain infections

A

No need to cross BBB to cause disease

106
Q

Acute flaccid myelitis

A

Infection of the spinal cord

107
Q

Brain barriers to infection

A

Physical protection - skull/vertebrae, meninges, CSF
Brain-CSF barrier
BBB
Olfactory portal

108
Q

Mechanism of bacterial invasion of blood-brain & blood-CSF barriers

A

Transcellular penetration
Paracellular entry
“Trojan horse” mechanism

109
Q

What protects the brain from infection?

A

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
Q

Treatment of trigeminal neuralgia

analgesics

A

Carbamazepine

111
Q

MOA of antipsychotics

A

Inhibit dopamine D2 receptors

MBBS (28 decks)

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