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Pharmacology Flashcards

1
Q

What are the 4 types of dementia?

A

Alzheimer’s
Fronto-temporal
Vascular (unusually associated with damage)
Dementia with Lewy bodies (associated with Parkinson’s disease)

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2
Q

What are the characteristics of frontotemporal dementia?

A
  • associated with early onset dementia
  • global cognitive impairment and motor deficits with are fatal with death occurring after around 8 years after symptom onset
  • symptoms: progressive deterioration of behaviour with behavioural disinhibition, loss of sympathy and empathy, compulsive/ritualistic behaviour, dietary changes (e.g. consumption of inedible objects, altered food preferences)
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3
Q

What are the characteristics of dementia with Lewy bodies? (DLB)

A
  • characteristics shared between Alzheimer’s Disease and Parkinson’s disease
  • formations of Lewy bodies containing alpha-synuclein thought to originate within the brain stem, progressing ti the limbic system and cerebral cortex
  • symptoms: dementia and delirium-like changes in cognition, visual hallucinations, rapid eye movements
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4
Q

Characteristics of vascular dementia?

A
  • Associated with demographic, genetic, atherosclerotic and stroke relative risk factors
  • Pathological hallmark; not yet determined due to variable cognitive impairment that is less sensitive to cognitive tests
  • Symptoms: varies memory impairment
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5
Q

What are the macroscopic pathology features of Alzheimer’s Disease (AD)?

A
  • Moderate cortical atrophy within cortex and limbic system
  • Enlarged frontal and temporal horns of the lateral ventricles
  • Widening of sulcal spaces and narrowing of gyro compared to normal brain
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6
Q

What are the microscopic pathology features of AD?

A

-Amyloid plaques- Formed from accumulation of Abeta40 and Abeta42
Abeta42 is prominent and dominant in the formation of amyloid plaques in AD
These plaques are associated with neuronal loss and cognitive decline
- Neurofibrillary tangles: composed of filamentous tau protein. In AD tau proteins are hyperphosphorylated and abnormally folded, leading to loss of tau function - compromised normal tau protein leads to the spread of tau pathology in the AD brain

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7
Q

Which allele of apolipoprotein E (APOE) is associated with AD risk?

A

E4

  • around 3 fold risk if inherit one cope of e4 (APOE4 heterozygous)
  • around 15 fold risk if inherit 2 (homozygous APOE4)
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8
Q

What are the 4 symptomatic treatments of dementia?

A
  1. Augmenting the cholinergic pathways - e.g. cholinesterase inhibitors
  2. NMDA receptor antagonists
  3. Management of behavioural and psychological symptoms - pharmacological and non-pharmacological
  4. Palliative care at end stage disease
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9
Q

How do acetylcholinesterase inhibitors work in treating dementia?

A

Block eat erase-mediated metabolism of ACh to choline and acetate which results in increased ACh availability for postsynaptic and presynaptic nicotinic and muscarinic ACh receptors

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10
Q

How do glutamate modulators (NMDA a N-methyl-D-Asperate) receptor antagonists work?

A

Memantine
Replacement of glutamine in NDMA receptor binding which reduces AD symptoms and disease
Used as an alternative to ACHE inhibitors due to intolerance or counter indications

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11
Q

What is a seizure?

A

A transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

  1. Clinical manifestation
  2. Discorded and hypersynchronised discharge
  3. In a network of cerebral neurons
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12
Q

What is epilepsy?

A

A pathological and enduring tendency to have recurrent seizures and by the neuro-biological, cognitive, psychological, and social consequences of his condition

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13
Q

What are the two main types of seizure?

A
  1. Generalised seizures - starts simultaneously in both hemispheres
  2. Focal seizures - seizure starts in a focus and then spreads
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14
Q

What are the common generalised seizures?

A

Typical absence, myoclonic, tonic-clonic

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15
Q

Describe a myoclonus seizure

A

Sudden, brief, shock-like muscle contractions. Usually bilateral arm jerks and often worse in mornings. Precipitated by sleep deprivation and alcohol

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16
Q

Describe tonic-clonic seizures

A

Sudden onset, gasp, fall. Tonic phase with cyanosis (lips go blue). Clonic phase and a post ictal phase (altered state of consciousness after an epileptic seizure). Tongue bitten and incontinence, noisy breathing, headache and muscle pain afterwards

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17
Q

What are the uncommon generalised seizures?

A

Atypical absence, tonic, atonic (usually associated with severe epilepsy

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18
Q

Describe focal seizures

A

Focal onset - often aura or “warning” at onset
As seizures spreads - loss of awareness and involuntary movement
Often caused by brain lesions

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19
Q

Describe temporal lobe seizures

A

Auras- rising sensation in stomach, olfactory and gustatory hallucinations (smell or taste), déjà vu
As seizure spreads - suddenly stops and blank stares, loss of responding and awareness, mouth movements, fidgeting or postures, automatisms (nonpurposeful, stereotyped, and repetitive behaviours following a seizure)

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20
Q

What can epileptiform discharges be due to?

A
  • Neuronal bursting (an ion channel property)
  • Synaptic effects (both glutamate and GABA)
  • Glia effects
  • Non-synaptic effects (e.g. extra cellular K+)
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21
Q

What changes occur in the epileptogenesis model?

A

Structural: Cell loss inhibitory (interneurons) - disinhibition circuits
Axonal sprouting - extra excitatory circuits
Neurogenesis
Gliosis (glial reaction in response to damage)
Neuro-inflammation
Molecular: neuronal channels (Na, K, Ca, Cl, HCO3-) “acquired channelopathy”
Receptors - GABA, AMPA, NMDA, ACh
Neurotransmitter transporters
Neuro-modulators (peptides + endocannabinoids)
Functional: gap junctions, glia: buffering of extra cellular environment
Blood brain barrier breakdown

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22
Q

What activity occurs in the prefrontal cortex?

A

Intellectual function; emotional behaviour (suppresses aggressive behaviour

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23
Q

What activity occurs in the motor cortex?

A

Contains the premotor and primary motor cortex

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24
Q

Which part of the brain governs the sleep-wake cycle?

A

The suprachiasmatic nucleus (SCN) present within the hypothalamus

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25
Q

What happens during non-REM sleep (NREM)?

A

Restful and restorative
Stage 1: transition from awake to sleep
Stage 2: initiate ‘true’ sleep
Stage 3 and 4: deep sleep

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26
Q

What happens during REM sleep?

A

Consolidate and integrate memories
Development of CNS
Presents with burst of rapid eye movements
Other physiological processes

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27
Q

Name 5 neurochemical systems that promote arousal

A
  1. Ach: forebrain and brainstorm, active during wakefulness and REM sleep
  2. NA/NE: generate arousal ‘fight/flight response’
  3. Histamine: promotes wakefulness; reducing REM & NREM
  4. 5-HT: promotes wakefulness and suppresses REM sleep
  5. DA: exerts potent wake promoting effects
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28
Q

Name 5 types of sleep disorders

A
  1. Rapid eye movement disorder
  2. Restless legs syndrome
  3. Periodic limb movement of sleep
  4. Insomnia
  5. Excessive daytime sleepiness
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29
Q

What are the symptoms and potential causes of restless leg syndrome?

A
  • uncomfortable feeling in the legs and feet (itchy, twitchy, throbbing etc)
  • powerful urge to move legs to reduce the uncomfortable feeling
  • worsening at night when lying or sitting

Causes: dopamine dysfunction, genetics, medications, chronic illness, vitamin and mineral deficiency (B12, magnesium), pregnancy (3rd trimester), sleep deprivation

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30
Q

What is multiple sclerosis?

A

Demyelinating disease, autoimmune disease, inflammatory disease
Immune cells attack myelin - inflammatory response - myelin debris accumulates in lesions with causes and immune response

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31
Q

What and the genetic and environmental factors that lead to MS?

A
  • Autoimmune diseases more common where people don’t experience extreme hunger
  • family link increases odds by 40%
  • 2-3 fold increased prevalence in women
  • Caucasian/ northern hemisphere bias
  • triggering infection (similar antigen?)
  • vitamin D deficiency
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32
Q

What are the 4 types of MS?

A
  1. Relapsing Remitting MS (RRMS) - most common (85% of cases). Discrete attacks that evolve over days or weeks followed by some degree of recovery over weeks or months. In between attacks the patient has no worsening neurological function
  2. Secondary progressive MS (SPMS) - initial relapse followed by gradual neurological deterioration not associated with acute attacks
  3. Primary progressive MS (PPMS) - steady functional decline from the onset of the disease. No relapses ever
  4. Progressive relapsing MS (PRMS) - steady functional decline from onset of the disease with later superimposed acute attacks. PRMS and PPMS cannot be distinguished during early stages, until relapse occurs
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33
Q

What is the autoimmune cascade at MS lesions?

A
  1. microglia an/or macrophages erroneously respond to myelin basic protein as an antigen
  2. Local innate immune response (release cytokines, pro-inflammatory mediators, and cytotoxic agents such as superoxide and nitric oxide)
  3. Antigen presenting cells recruit T cells and B cells from circulation
  4. Full immune response involving complement, antibodies, cytokines and chemokines
  5. microglia and astrocytes isolate lesion via reactive gliosis
  6. Anti-inflammatory T cells terminate the response
  7. Episode (hopefully) resolves
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34
Q

What happens when the membrane depolarises?

A

Depolarization opens sodium ion channels (fast)
Sodium ions flood into the cell down its electrochemical gradient
This depolarizes the membrane even more

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35
Q

How is the membrane repolarised?

A

potassium ion channels open (more slowly) and flood out of the cell down its electrochemical gradient.
Sodium ion channels inactivate preventing further depolarisation
This repolarises the membrane

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36
Q

What are the symptoms of MS?

A 
Disrupted vision
Tingling, numbness, pain
Muscle spasm or weakness (speech impairment)
Loss of coordination
Loss of bladder/bowel control
Fatigue 
Cognitive impairment
Mood changes
Can lead to severe disability
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37
Q

What treatments can be used? (3 approaches)

A
  1. Manage the symptoms ( visual: gabapentin, ophthalmological treatments. Muscle spasms/stiffness: baclofen, gabapentin, diazepam. Pain: gabapentin, carbamazepine, amitriptyline and physiotherapy and lifestyle changes)
  2. Speed recovery during relapse (high dose corticosteroids e.g. methylprednisolone to supress inflammatory response and speed resolution of relapse episode)
  3. Slow the progression (disease-modifying therapies - immunomodulating drugs and biologics work by suppressing autoimmune response e.g. beta interferons, glatiramer acetate, fingolimod, ocrelizumab, alemtuzumab, cladribine, dimethyl fumarate, haematopoietic stem cell transplantation aka chemotherapy)
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38
Q

Explain how beta-interferons work

A
  • cytokines released from fibroblasts as part of antiviral immune response
  • inhibit activation and migration of T cells
  • suppress the release of pro-inflammatory cytokines
  • slows disease progression
  • subcutaneous or intramuscular dosing
  • decreases frequency and severity of relapses
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39
Q

Explain how glatiramer acetate works

A
  • a random polymer of amino acids (immune decoy?)
  • activates regulatory T cells that suppress the inflammatory response
  • may also destroy pro-inflammatory T cells
  • shifts balance of innate immune response from pro-inflammatory to anti-inflammatory state
  • subcutaneous injection
  • decreases number of relapses
  • slows progression of disease
40
Q

What are the three main dopamine pathways?

A
  1. Nigrostriatal pathway (Parkinson’s disease)
  2. Mesocortical and mesolimbic pathways (schizophrenia)
  3. Tuberoinfundibular pathway (prolactin release - unaltered in psychosis)
41
Q

What are the structural brain changes seen in schizophrenia?

A
  • enlargement of the lateral ventricles
  • a slight decrease in size of the brain
  • histology: altered neuronal and synaptic organisation, affected white matter, no gliosis = absence of neurodegenerative process

schizophrenia is neurodevelopmental not neurodegenerative

42
Q

How do antipsychotics work?

A
  • block post-synaptic dopamine (D2) receptors in three pathways:
    1. mesocortical/mesolimbic = antipsychotic effect
    2. nigrostriatal = movement side-effects (extrapyramidal side effects EPSA) - may need to switch to a different antipsychotic or lower dose as can be like a Parkinsons temor
    3. tuberoinfundibular = hyperprolactinaemia

This is because increases dopamine activity in mesocortical and mesolimbic area of the brain is linked to “positive” psychotic symptoms

43
Q

What is Tardive Dyskinesia (TD)?

A
  • Facial and tongue movements, grimacing, lip-smacking, and quick jerky limb movements
  • can be irreversible and quick recognition is essential
  • usually due to long-term use of FGAs (first-generational antipsychotics)
  • possibly due to up-regulation and increased DA receptor sensitivity in the nigrostriatal pathway
44
Q

How does dopamine affect prolactin?

A

dopamine stops release of prolactin from the pituitary

dopamine blockage results in prolactin release and hyperprolactinemia

45
Q

What are the consequences of raised prolactin?

A
  • galactorrhoea (milky nipple discharge unrelated to the normal milk production of breastfeeding)
  • amenorrhoea (absence of menstrual period)
  • interference with fertility
  • gynaecomastia (‘man boobs’)
  • sexual dysfunction
  • demineralization of bones
  • weight gain
46
Q

What are the different types of stroke?

A
47
Q

What are the symptoms of stroke?

A
  • haemorrhage: thunderclap headache, seizures, nausea, unilateral weakness
  • anterior circulation: hemiplegia/paresis, hemisensory loss, hemianopia (loss of vision in one eye), dysphagia, aphasia
  • posterior circulation: bilateral sensory/motor deficits, dis-conjugate eye movement, cerebellar dysfunction, isolated hemianopia
  • non-specific symptoms: confusion, drowsiness, dizziness, nausea, double vision, incontinence
48
Q

What is a lacunar infarction?

A
  • small, strategic strokes in penetrating arteries that feed sub-cortical structures
  • 80% can be clinically silent
  • motor hemiplegia syndrome: infarction in the posterior limb of the internal capsule, basal ganglia, or pons
49
Q

What is the most common type of stroke?

A

middle cerebral artery infarction, which results in contralateral hemiplegia and hemisensory loss

50
Q

How can cell fate be dictated following a stroke?

A

There are cerebral blood flow thresholds that dictate cell fate
The core represents irreversibly damaged tissue
The penumbra represents potentially salvageable tissue

51
Q

What is the immediate treatment of stroke?

A

300mg aspirin within 24 hours for up to 2 weeks

Patients may also take anticoagulation medication such as warfarin or dabigatran

52
Q

What medications can be used to lower blood pressure?

A 
diuretics 
calcium channel blockers 
beta-blockers
angiotensin-converting-enzyme inhibitors 
angiotensin receptor blockers 
alpha blockers
53
Q

Where is the chemoreceptor trigger zone (CTZ)?

A

At the base of the forth ventricle - has multiple receptors (dopamine D2, 5-HT3, opioid and acetylcholine), a neurokinin (substance P) is the major output transmitter

54
Q

Where might the vomiting centre receive inputs to initiate the motor components of the vomiting reflex?

A

CTZ
a neurokinin (substance P)
the area postrema which detects blood chemicals (has no BBB)
the vestibular system via the vestibulocochlear (8th cranial) nerve - major role in motion sicknes - rich in muscarinic cholinergic and histamine H1 receptors
Vagal (10th cranial) nerve afferents activated when the pharynx is irritated, leading to the gag reflex - nucleus tractus solitarius has high density of 5-HT3 and NK1 receptors
vagal and other gastrointestinal afferents responding to irritation of the GI mucosa by chemotherapy, radiation, distention, or acute gastroenteritis via gut 5-HT3 receptors
Intercranial pressure receptors mediating nausea after head injury or meningitis
Descending inputs from higher centres arising from the sight or smell of vomit, situations associated with vomitting, psychiatric disorders, or with general stress

55
Q

What are the drugs used to control nausea or vomiting?

A

5HT3 antagonists (ondansetron, granistetron)
Eicosanoid synthesis inhibition - corticosteroid (dexamethasone)
Neurokinin 1 antagonist [agonist:substance P] (aprepitant, casopitant)
Dopamine D2 antagonists (metoclopramide, domperidone, haloperidol)
Muscarinic antagonist (scopolamine)
Antihistamines (cinnarizine)
Histamine H3 antagonists (btahistine: for vertigo nausea)
Cannabinoid agonists (nabilone)
Multiple [dopamine, 5HT & muscarinic antagonist] (olanzapine)

56
Q

What is the definition of Parkinson’s disease?

A

Neurodegenerative - death of dopamine-containing cells of the substantia nigra
Substantia nigra: origin of dopaminergic afferents implicated in Parkinson’s disease

57
Q

What is the pathophysiology of Parkinson’s disease?

A

Dopamine neuron loss in substantia nigra
Loss of noradrenergic, serotonegic and cholinergic neurons also evident
Lewy bodies: accumulation of protein deposits in substantia nigra, locus coeruleus and other brain regions

58
Q

What are the motor symptoms of Parkinson’s disease?

A

Bradykinesia: slowness of movement
Resting tremor: shaking that disappears during active use of the affected body part
Rigidity: Increased resistance to passive movement
Postural instability: Instability when standing, or impaired balance and coordination; feature of more advanced disease

59
Q

What are the non-motor symptoms of Parkinson’s disease?

A
  • Sleep disorders: affects ~ 70% of patients. Insomnia, night terrors, restless leg syndrome
  • Autonomic disturbances: constipation, urinary incontinence, sexual dysfunction, orthostatic hypotension
  • Psychological symptoms: psychosis, dementia, depression, anxiety
60
Q

What are the recommended pharmacological management drugs for motor symptoms in PD?

A
  • Levodopa
  • Dopamine agonists
  • Monoamine oxidase type-B inhibitors & catechol-0-methyl transferase
  • Amantadine (less commonly used)
61
Q

Explain Levodopa (L-dopa)

A
  • precursor of dopamine
  • administered with carbidopa (peripheral dopa decarboxylase)
  • long term use associated with motor complications mainly dyskinesia and on-off motor fluctuations

Dyskinesia: involuntary movements - similar to ‘tics’, occur when drug is at peak dose so consider reducing
On-off motor effects: seen in advanced PD, ‘on’ = motor symptoms well controlled and ‘off’ = rapid L-dopa wearing off so effects fluctuate

62
Q

How do dopamine agonists work?

A
  • bind to dopamine receptors
  • prescribed in younger patients to delay L-dopa use
  • common side effects: nausea and vomiting, dry mouth, insomnia, constipation, etc…
  • adverse effect: patients may develop compulsive and behavioural problems
63
Q

How do monoamine oxidase B (MAO-B) inhibitors work?

A
  • inhibit dopamine metabolism
  • relieves motor symptoms
  • can be used together with dopamine agonists to delay levodopa use
  • mainly controls symptoms in early disease, with most patients ultimately needing levodopa
  • catechol-0-methyl transferase inhibitors - similar to MAO-B inhibitors
64
Q

How does Amantadine work?

A
  • initially used as an anti-viral drug for treating flu
  • short-lived improvement in symptoms which is of benefit if a lower dose of levodopa is needed
  • limits levodopa-induced dyskinesias
  • mechanism of action unclear with proposed mixed dopaminergic and anti-glutamatergic actions
65
Q

When might surgical management of PD be used?

A
  • no evidence of significant cognitive decline, hallucinations, dementia, or severe depression
  • have severe motor fluctuations including dyskinesia
  • depends on response to dopaminergic medications
  • is the patient well enough to attend surgery?
66
Q

How is PD surgically managed?

A
  • permanent implantation of leads into the subthalamic nucleus, thalamus or globus pallidus
  • leads deliver high frequency electrical impulses controlled by stimulatory
  • shown to alleviate motor symptoms
  • presents opportunity to decrease levodopa dose
67
Q

Function of sensory neuron

A

transmitting impulses from the periphery to CNS e.g. pain, tactile information etc

68
Q

Role of motor neuron?

A

a nerve cell forming part of a pathway along which impulses pass from the brain or spinal cord to a muslce or gland

69
Q

Role of interneurons?

A

form the connection between sensory and motor neurons (AKA as a relay neuron)

70
Q

Role of astrocytes?

A

jack of all trades - mainly maintains the BBB

71
Q

Role of oligodendrocytes?

A

support the neurones structurally

72
Q

Role of microglia?

A

mop up the dead debris, basically getting rid of dead neurons and glial cells through the proess of phagocytosis

73
Q

What protects the brain from damage?

A

the meninges

74
Q

What is the subarachnoid space?

A

layer between arachnoid and pia mater

75
Q

What is the brain made of?

A

Brain ventricles which are filled with cerebrospinal fluid (CSF)

76
Q

How is CSF produced?

A

by the choroid plexus cells which are present in the lateral, third and fourth ventricles

77
Q

How and when is the CNS formed?

A

starts in 2-3 week embryo
process commences with the neural tube which invaginates (folds in on itself) eventually developing into the midbrain, forebrain and hindbrain which you can clearly see takes shape over the course of a couple of months
Fully formed by birth

78
Q

What is anencephaly?

A

baby is born without parts of the brain and skull
prevented by folic acid treatment in pregnancy
no treatment and baby dies shortly after birth

79
Q

How are neurons and glial cells formed?

A
80
Q

What are the three main areas of the brainstem and their function?

A

Medulla: centre for respiration and circulation
Pons: bridge between different brain regions; assist in controlling autonomic function; sleep and arousal
MIdbrain: controls body movement; location for substantia nigra; relay auditory and visual information

81
Q

Function of cerebellum?

A

‘little brain’

coordinated fine muscle movement and balance and if damaged can lead to ataxia

82
Q

Function of hypothalamus?

A

Integrated function: regukates cardiovascular & temperature, feeding & drinking, sexual behaviour, sleep, aggression etc
Gives rise to the pituitary gland which is repsonsible for release of hormones

When it goes wrong: cannabis munchies, erectile dysfunction, anorexia, diabetes insipidus, developmental disorders

83
Q

Function of the thalamus?

A

Brain’s sensory switchboard

Relays sensory information to and from the cortical regions

84
Q

Function of corpus callosum?

A

Connects the left and right hemispheres of the brain
absense would mean seizures, delays in movement - symptom severity depends on the extend of disconnect - treated by seizure meds of physical therapy

85
Q

Function of cerebral cortex?

A

Largest and most developed part of the brain split into 4 lobes (frontal, parietal, occupital and temporal)
Responsible for thinking, perceiving, producing and understanding language

86
Q

Function of frontal lobe?

A

Prefrontal cortex: intellectual function; emotional behaviour (supresses aggressive behaviour)
Motor cortex: contains the premotor and primary motor cortex

87
Q

Function of parietal lobe?

A

Processes sensory information associated with tatse, temp, touch; knowledge of numbers; orientation etc

88
Q

Function of occipital lobe?

A

COncerned with processing visual info

89
Q

Function of temporal lobe?

A

Contains the primary auditory cortex

Some visual cognition due to close association with the occipital lobe

90
Q

Function of basal ganglia?

A

Associated with the cerebral cortex
Initiates and coordinates activities such as walking
Inhibits unwanted movements or unnecessar movements
In PD movement control is disrupted due to death of basal ganglia neurones

91
Q

Explain the limbic system

A

The emotion
Divided into cortical and subcortical portions
Cortical portion: includes hippocampus, parhippocampal gyrus and cingulate gyrus and they surround the corpus callosum
The subcortical regions include the amygdala, hypothalamus and the anterior thalamic nuclei

92
Q

Function of hippocampus?

A

Long term memory
The hippocampus has also been found to be involved in the learning and storage of information referring to space - spatial navigation
Associated with Alzheimers disease
Associate with inhibition of behaviour found as leading to consequences

93
Q

Function of cingulate gyrus?

A

Coordinates sensory input with emotions
Connected to the hippocampus and hypothalamus and its main role is to coordinate information related to emotions and to some extent pain

94
Q

Function of amygdala?

A 
Anger
agression
fear
sex drive
memory
anxiety
sadness
binge drinking?
95
Q

Excitatory neurotransmitter?

A

Glutamate releasing sodium into postsynaptic neuron

96
Q

Inhibitory neurotransmitter?

A

GABA releasing chloride io into postsynaptic neuron

CNS (4 decks)

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