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Psychiatry > Basic Science & Pharmacology > Flashcards

Basic Science & Pharmacology Flashcards

1
Q

Definition of prolonged QTc

A

> 460 (prepubertal)
470 (postpubertal men)
480 (postpubertal women)

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2
Q

How neurons communicate with each other

A

Neurotransmitters made from amino acids

  • -> collected into vesicles by VMAT (vesicular monoamine transporter)
  • -> vesicles release neurotransmitters into synaptic cleft
  • -> neurotransmitters bind to postsynaptic receptor or presynaptic autoreceptor
  • -> stimulation of postsynaptic receptor causes inhibitory or excitatory postsynaptic potential
  • -> sum of excitatory and inhibitory postsynaptic potential at axon hillock crosses depolarization threshold
  • -> action potential sent down axon
  • -> influx of calcium causes vesicular release of neurotransmitter into synaptic cleft

–> monoamines reuptaken by transporter protein or broken down (in synaptic cleft or in presynaptic neuron)

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3
Q

Types of CNS cells

A

Pyramidal neurons

Glial cells

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4
Q

Definition of glial cells

A

Non-neuron CNS cells

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5
Q

Types of glial cells

A

Oligodendocytes
Microglia
Astrocytes

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6
Q

Function of oligodendrocytes

A

Akin to Schwann cells in PNS (provide myelin sheath for neurons in CNS)

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7
Q

Function of microglia

A

“Macrophages” of CNS (clean up cellular debris)

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8
Q

Function of astrocytes

A

Provide nutrients to neurons
Provide structural support for neurons/capillaries
Modulate synaptic activity
Regulate CSF composition

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9
Q

Main inhibitory neurotransmitter

A

GABA

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10
Q

Role of GABA

A

Main inhibitory neurotransmitter

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11
Q

Main excitatory neurotransmitter

A

Glutamate

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12
Q

Role of glutamate

A

Main excitatory neurotransmitter (and main neurotransmitter in brain overall; 80% of synapses)

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13
Q

Types of monoamines

A 
Dopamine
Serotonin
Norepinephrine
Epinephrine
Acetylcholine
Histamine
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14
Q

Types of catecholamines

A

Dopamine
Norepinephrine
Epinephrine

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15
Q

Production of dopamine and NE/epinephrine

A

Phenylalanine –> tyrosine –> tyramine –> L-DOPA –> dopamine –> NE –> epinephrine

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16
Q

Which molecule causes hypertensive crisis with MAOIs

A

Tyramine

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17
Q

Production of serotonin

A

Tryptophan –> 4-HT –> 5-HT (serotonin)

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18
Q

Production of melatonin

A

Tryptophan –> melatonin

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19
Q

What’s special about tryptophan

A

Produced into serotonin + melatonin

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20
Q

What foods are tryptophan found

A

Milk, turkey

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21
Q

What does MAO-A do

A

Break down serotonin and NE

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22
Q

What does MAO-B do

A

Break down dopamine and histamine

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23
Q

Function of dopamine

A

Increase reward seeking
Assign importance to rewarding environmental stimuli
Inhibits prolactin release

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24
Q

Where are dopaminergic neurons clustered

A 
Ventral tegmental area (midbrain)
Substantia nigra (basal ganglia structure in midbrain)
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25
Q

Main dopaminergic pathways

A

Mesolimbic
Mesocortical
Nigrostriatal
Tuberoinfundibular

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26
Q

Clinical significance of mesolimbic pathway

A

Excess dopamine = positive symptoms of schizophrenia

Main pathway in reward system

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27
Q

Clinical significance of mesocortical pathway

A

Insufficient dopamine = negative symptoms of schizophrenia

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28
Q

Clinical significance of nigrostriatal pathway

A

Insufficient dopamine = extrapyramidal symptoms

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29
Q

Clinical significance of tuberoinfundibular pathway

A

Insufficient dopamine = hyperprolactinemia

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30
Q

Where does mesolimbic pathway connect to/from

A

Ventral tegmental area (VTA; in midbrain) –> nucleus accumbens + amygdala

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31
Q

Where does mesocortical pathway connect to/from

A

Ventral tegmental area (VTA; in midbrain) –> prefrontal cortex

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32
Q

Where is ventral tegmental area located

A

Midbrain

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33
Q

Main dopamine receptor

A

D2 receptor

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34
Q

Clinical significance of D2 receptors

A

Antipsychotics = D2 antagonists

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35
Q

Where noradrenergic neurons predominately found

A 
Locus ceruleus (dorsal caudal pons) 
Lateral tegmental noradrenergic nuclei (in ventral pons and medulla)
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36
Q

Caudal

A

Inferior (“cauda equina” = horse tail)

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37
Q

Dorsal

A

Back (dorsum of hand)

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38
Q

Where is locus ceruleus located

A

Dorsal caudal pons (inferior/posterior part of pons)

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39
Q

Where is epinephrine released

A

Adrenal medulla (inner section)

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40
Q

Types of adrenergic receptors

A

Alpha 1 and 2

Beta 1 and 2

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41
Q

Clinical significance of alpha-2 receptors

A

Autoreceptor for presynaptic adrenergic neurons –>

Reduce sympathetic and increase parasympathetic activity

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42
Q

Clinical significance of beta-2 receptors

A

Beta-2 agonists = bronchodilators (e.g. Ventolin)

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43
Q

Serotonergic neurons predominately found in

A

Raphe nuclei (in midbrain)

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44
Q

Where are raphe nuclei found

A

Midbrain

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45
Q

Location of serotonin receptors

A

80% GI system
Platelets
2% CNS (raphe nuclei in midbrain)

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46
Q

Clinical significant of 5-HT1 receptor

A

Inhibitory autoreceptor for serotonergic neurons
Modulates anxiety/depression
Triptans = 5HT1 B/D antagonist

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47
Q

Clinical significance of 5-TH2A receptor

A

Atypical antipsychotics = 5HT2 antagonist

LSD = 5HT2 agonist

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48
Q

Clinical significance of 5-HT2C receptor

A 
Anxiogenic effects (creates anxiety)
Role in weight gain + T2DM w/ atypical antipsychotics
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49
Q

Clinical significance of 5-HT3 receptor

A

Ondansetron = 5HT3 agonist

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50
Q

Types of cholinergic receptors

A

Muscarinic

Nicotinic

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51
Q

Cholinergic neurons predominately found in

A

Basal forebrain complex

Mesopontine complex

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52
Q

Histaminergic neurons predominately found in

A

Tuberomammillary nucleus in posterior hypothalamus

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53
Q

Where tuberomammillary nucleus found

A

Posterior hypothalamus

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54
Q

Clinical significance of raphe nuclei

A

Contains most serotonergic neurons

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55
Q

Clinical significance of ventral tegmental area

A

Contains most dopaminergic neurons

along with substantia nigra

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56
Q

Clinical significance of substantia nigra

A

Contains most dopaminergic neurons
Part of basal ganglia

(along with ventral tegmental area)

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57
Q

Clinical significance of locus ceruleus

A

Contains most adrenergic neurons

along with lateral tegmental noradrenergic nuclei

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58
Q

Clinical significance of lateral tegmental noradrenergic nuclei

A

Contains most adrenergic neurons

along with locus ceruleus

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59
Q

Clinical significance of tuberomammillary nucleus

A

Contains most histaminergic neurons

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60
Q

Where histamine predominately found

A

Mostly mast cells

CNS (in tuberomammillary nucleus)

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61
Q

Role of histamine

A

Allergic reaction (inflammatory mediator)
Modulates sleep-wake cycle (highest during awake state)
Modulates feeding behaviour

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62
Q

Types of histaminergic receptors

A

H1

H2

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63
Q

Clinical significance of H1 receptors

A

Allergy meds = H1 antagonist

Antagonism = sedation, weight gain

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64
Q

Clinical significance of H2 receptors

A

H2 blockers = ranitidine (peptic ulcer, GERD)

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65
Q

Main glutamate receptor

A

NMDA receptor

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66
Q

Main GABA receptor

A

GABA A receptor

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67
Q

Divisions of nervous system

A

CNS

PNS

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68
Q

Divisions of CNS

A

Brain

Spinal cord

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69
Q

Divisions of brain

A

Cerebrum
Cerebellum
Brainstem

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70
Q

Divisions of brainstem

A

Midbrain
Pons
Medulla

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71
Q

Divisions of peripheral nervous system

A 
Sensory (afferent) NS
Motor (efferent) NS
- Somatic NS (voluntary movements)
- Autonomic motor NS (involuntary movements)
     - Sympathetic NS
     - Parasympathetic NS
72
Q

Difference betw somatic and autonomic NS

A 
Somatic = voluntary movements
Autonomic = involuntary movements
73
Q

Structure that connects two hemispheres

A

Corpus callosum

74
Q

Corpus callosum

A

Structure that connects two hemispheres

75
Q

Diencephalon

A 
-thalamus structures including
Thalamus
Hypothalamus
Subthalamus
Epithalamus
Dorsal thalamus
76
Q

4 lobes of brain

A

Frontal
Temporal (side)
Parietal (upper middle)
Occipital

77
Q

Function of hypothalamus

A

Regulates homeostasis (temperature, satiety, hunger, BP, perspiration, sexual drive)
Regulates sleep wake cycle (suprachiasmatic nucleus in anterior hypothalamus)
Regulates hormone release from pituitary gland

78
Q

Indentation between frontal and parietal lobe

A

Central sulcus of Rolando

79
Q

Central sulcus (of Rolando)

A

Indentation betw frontal lobe and parietal lobe

80
Q

Indentation betw 2 hemispheres

A

Falx cerebri

81
Q

Falx cerebri

A

Indentation betw 2 hemispheres

82
Q

Indentation betw temporal lobe and frontal/parietal lobe

A

Lateral sulcus (aka Sylvian fissure, lateral fissure of Sylvius)

83
Q

Sylvian fissure

A

Indentation betw temporal lobe and frontal/parietal lobe

aka lateral sulcus, lateral fissure of Sylvius

84
Q

Composition of primitive reflex arc

A

Sensory neuron directly synapses on motor neuron

85
Q

Divisions of spinal nerves

A 
C1-8
T1-12
L1-5
S1-5
Coccygeal nerve
86
Q

Difference betw L and R hemisphere

A

R hemisphere = more emotionally adept

L hemisphere = more analytical

87
Q

Which side stroke more likely to get depression

A

L hemisphere stroke (R hemisphere more emotionally adept = still intact)

88
Q

Basic functions of frontal lobe

A

Voluntary motor control (motor strip)

Executive functions

89
Q

Definition of executive functions

A

Higher order cognition

Executing goal-directed activity

90
Q

Types of executive function skills

A 
"SOAP ME"
Sequencing
Organizing (incl time management) 
Abstract thinking (including perspective taking) 
Attention 
Planning
Motivation / initiation of tasks 
Emotion regulation / impulse control
91
Q

Components of frontal lobe

A

Motor strip
Supplemental motor area
Broca’s area
Prefrontal cortex

92
Q

Components of prefrontal cortex

A

Dorsolateral prefrontal cortex (top)
Medial prefrontal cortex (aka ventromedial prefrontal cortex; ventral = bottom)
Orbitofrontal prefrontal cortex (bottom lateral)
Anterior cingulate cortex

93
Q

Types of frontal lobe syndromes

A

“SOAP ME”
Disorganized = SOAP
Apathetic = M
Disinhibited = E

94
Q

Disorganized frontal lobe syndrome associated with what lesion

A

“SOAP ME” = top

Dorsolateral prefrontal cortex

95
Q

Dorsolateral prefrontal cortex associated with which frontal lobe syndrome

A

Dorsolateral PFC = top most = “SOAP ME”

Disorganized

96
Q

Apathetic frontal lobe syndrome associated with what lesion

A

“SOAP ME” = middle outer = medial prefrontal cortex

97
Q

Medial prefrontal cortex associated with which frontal lobe syndrome

A

Medial PFC = middle = “SOAP ME”

Apathetic

98
Q

Disinhibited frontal lobe syndrome associated with what lesion

A

“SOAP ME” = bottom = orbitofrontal prefrontal cortex

99
Q

Orbitofrontal prefrontal cortex associated with what frontal lobe syndrome

A

Orbitofrontal PFC = bottom most = “SOAP ME”

Disinhibited

100
Q

Basic functions of parietal lobe

A

Process sensory information (somatosensory cortex)
Attention
Visuospatial

101
Q

Basic functions of temporal lobe

A

Memory/learning

Processing auditory information

102
Q

Basic functions of occipital lobe

A

Processing visual info

103
Q

Lesion of movement disorders

A

Basal ganglia

104
Q

Role of basal ganglia

A

Smooth out voluntary movements

105
Q

Neurotransmitters associated with basal ganglia

A

Dopamine

Acetylcholine

106
Q

Nigrostriatal pathway connects to/from

A

Substantia nigra (basal ganglia structure in midbrain) to dorsal striatum

107
Q

Components of basal ganglia

A 
Caudate nucleus
Putamen ("caudate head rests head on pillow")
Globus pallidus external and internal 
Substantia nigra (in midbrain)
Subthalamus

(Claustrum, amygdala)

108
Q

Location of substantia nigra

A

Basal ganglia structure in midbrain

109
Q

Location of lesion in Parkinson’s disease / parkinsonism

A

Substantia nigra (think nigrostriatal pathway)

110
Q

Corpus striatum

A

Caudate nucleus + putamen + globus pallidus + internal capsule

111
Q

Striatrum

A

Caudate nucleus + putamen

112
Q

Lenticular nucleus

A

Putamen + globus pallidus

113
Q

Clinical significance of caudate nucleus

A

Part of basal ganglia
Inadequate activity = OCD, tic disorders
Lesion = Huntington’s

114
Q

Location of lesion with Huntington’s disease

A

Caudate nucleus

115
Q

Location of lesion with Wilson’s disease

A

Globus pallidus

think Wilson’s disease aka hepatolenticular i.e. lenticular nucleus = globus pallidus + putamen

116
Q

Clinical significance of globus pallidus

A

Part of basal ganglia

Lesion = Wilson’s disease, CO poisoning

117
Q

Pathway responsible for maintaining arousal

A

ARAS (ascending reticular activating system)

118
Q

Function of ascending reticular activating system

A

Maintaining arousal

119
Q

Function of limbic system

A

Linked to emotion

120
Q

Components of limbic system

A 
Amygdala
Hippocampus 
Fornix
Mamillary body 
Cingulate cortex 
Septal nuclei

Other (parahippocampal gyrus, hypothalamus, basal forebrain, nucleus accumbens, orbitofrontal cortex)

121
Q

Function of amygdala

A

Assigns emotional importance to experiences and regulates hippocampal activity accordingly (emotional events easier to remember)
Linked to fear/anxiety

122
Q

Papez circuit

A

Part of limbic system

Hippocampus + fornix + mamillary body + anterior nucleus of thalmus + cingulate gyrus

123
Q

Reward center of brain

A

Nucleus accumbens

124
Q

Clinical significance of nucleus accumbens

A

Reward center of brain

Part of mesolimbic pathway

125
Q

Main pathways of reward system

A

Mainly mesolimbic pathway

Also mesocortical pathway

126
Q

Clinical significance of basal forebrain

A

Basal forebrain complex stores most cholinergic neurons
Main structure with memory
Part of limbic system

127
Q

Brain structures important for memory formation

A

Amygdala
Hippocampus
Basal forebrain
Certain diencephalic nuclei

128
Q

Function of hippocampus

A

Converts short term to long term memory

129
Q

What is astereognosis

A

Inability to recognize objects based on touch

130
Q

Location of lesion with astereognosis

A

Somatosensory cortex

Inability to recognize objects based on touch

131
Q

Inability to recognize objects based on touch

A

Astereognosis

132
Q

What is prosopagnosia

A

Inability to recognize faces

133
Q

Inability to recognize faces

A

Prosopagnosia

134
Q

Location of lesion with prosopagnosia

A

Disconnect from L inferior temporal cortices to visual association area in L parietal lobe

135
Q

Balint’s syndrome

A

Triad of optic ataxia, oculomotor apraxia (inability to direct gaze rapidly), and simultanagnosia (inability to integrate a visual scene to become part of a whole)

136
Q

Triad of optic ataxia, oculomotor apraxia (inability to direct gaze rapidly), and simultanagnosia (inability to integrate a visual scene to become part of a whole)

A

Balint’s syndrome

137
Q

What is simultanagnosia

A

Inability to integrate a visual scene to become part of a whole

138
Q

Inability to integrate a visual scene to become part of a whole

A

Simultanagnosia

139
Q

Gerstmann’s syndrome

A

Agraphia + acalculia (calculation difficulties), right-left disorientation, finger agnosia (can’t recognize own finger)

140
Q

Agraphia + acalculia (calculation difficulties), right-left disorientation, finger agnosia (can’t recognize own finger)

A

Gerstmann’s syndrome

141
Q

Location of lesion of Balint’s syndrome

A

Parietoccipital lobe

(Triad of optic ataxia, oculomotor apraxia (inability to direct gaze rapidly), and simultanagnosia (inability to integrate a visual scene to become part of a whole) = movement + vision problems)

142
Q

Location of lesion of Gerstmann’s syndrome

A

Temporooccipital lobe

(Agraphia + acalculia (calculation difficulties), right-left disorientation, finger agnosia (can’t recognize own finger))

143
Q

Steps for brain development

A
  1. Ectoderm –> neural plate –> folds into neural tube –> becomes CNS
  2. Neuroblasts (neural stem cells) multiple in ventricular zones and migrate up radial cells (specialized glial cells) to outer edge of cortex to differentiate and mature
  3. Neuron growth and branching
  4. Pruning of axons and synapses based on usage
  5. Myelination continues into adulthood
144
Q

Normal EEG findings

A

Awake EEG = predominately alpha waves + occasional beta waves
Sleep EEG = theta waves (drowsy) –> sporadic sharp waves –> sigma waves (aka sleep spindles; progress into sleep) –> delta waves (deep sleep)

145
Q

Generalized diffuse slowing on EEG

A

Nonspecific encephalopathy

146
Q

Focal slowing on EEG

A

Focal lesion / focal seizure

147
Q

Triphasic waves on EEG

A

50% hepatic encephalopathy

50% other toxic-metabolic encephalopathy

148
Q

Epileptiform discharges on EEG

A

Classic interictal finding for epilepsy

149
Q

Classic EEG finding for hepatic encephalopathy

A

Triphasic waves

150
Q

Hormones released by pituitary gland

A 
Anterior lobe 
- Thyroid stimulating hormone (TSH) 
- Growth hormone
- Luteinizing hormone (LH)
- Follicle stimulating hormone (FSH)
- Prolactin
- Adrenocorticotrophic hormone (ACTH)
Posterior lobe 
- Oxytocin
- Antidiuretic hormone (ADH)
151
Q

Anterior pituitary gland releases what hormones

A
  • Thyroid stimulating hormone (TSH)
  • Growth hormone
  • Luteinizing hormone (LH)
  • Follicle stimulating hormone (FSH)
  • Prolactin
  • Adrenocorticotrophic hormone (ACTH)
152
Q

Posterior pituitary gland releases what hormones

A
  • Oxytocin

- Antidiuretic hormone (ADH)

153
Q

Adrenal gland releases what hormones

A 
Cortex (outer section)
- Aldosterone
- Cortisol
- Testosterone
Medulla (inner section)
- Epinephrine
154
Q

Adrenal cortex releases what hormones

A
  • Aldosterone
  • Cortisol
  • Testosterone
155
Q

Adrenal medulla releases what

A

Epinephrine

156
Q

Function of sleep

A

Energy conservation
Tissue repair
Consolidate growth/learning
Remove neurotoxic metabolite waste products

157
Q

How light affects sleep-wake cycle

A

Blue light stimulates ganglion cells in retina –>
signal travels to anterior hypothalamus to suprachiasmatic nucleus (“master biological clock”)
–> stimulates pineal gland to release melatonin –> melatonin regulates circadian rhythm

158
Q

Clinical significance of suprachiasmatic nucleus

A

Master clock of circadian rhythm

159
Q

Master clock of circadian rhythm

A

Suprachiasmatic nucleus

160
Q

Location of suprachiasmatic nucleus

A

Anterior hypothalamus

161
Q

What sleep cycle is regulated by

A 
Process C (normal circadian rhythm) 
Process S (sleep homeostat; sleep debt; modulated by adenosine)
162
Q

Clinical significance of adenosine

A

Main neuromodulator for sleep debt (process S)

163
Q

Main neuromodulator for sleep debt

A

Adenosine

164
Q

MOA caffeine

A

Inhibits adenosine production (main neuromodulator for sleep debt)

165
Q

Stages of sleep cycle

A 
Stage 1 (drowsy)
Stage 2 (progression into sleep, less aware)
Stage 3 (previously stage 3+4) = deep sleep, slow-wave sleep 
REM (rapid eye movement) sleep
166
Q

Alpha waves on EEG

A

Predominant EEG finding when awake

167
Q

Beta waves on EEG

A

Associated with awake EEG

168
Q

Theta waves on EEG

A

Drowsiness

169
Q

Sigma waves

A

Stage 2 sleep (progression into sleep)

Aka sleep spindles

170
Q

Delta waves on EEG

A

Main finding with deep sleep

171
Q

Stage 2 sleep findings on EEG

A 
Sigma waves (aka sleep spindles) 
K complexes
172
Q

Stage 3 sleep findings on EEG

A

Delta waves

173
Q

Part of sleep associated with restorative sleep

A

Stage 3

old Stage 3+4; slow wave sleep

174
Q

Normal changes with sleep with aging

A

Advanced sleep phase (wake time + bedtime earlier)
Decreased need for sleep
Lighter sleep (i.e. less slow-wave (stage 3) sleep + REM sleep)
Decreased tolerance for dramatic phase shifts (e.g. jet lag)

175
Q

Acetylcholine is broken down by

A

Acetylcholinesterase in synaptic cleft

Psychiatry (8 decks)

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