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Genes and Behaviour > NBSS > Flashcards

NBSS Flashcards

1
Q

CN I

A

Olfactory nerve:
olfactory nerves –> olfactory bulb (cribriform plate) –> olfactory tract –> olfactory cortex (anterior ends of temporal cortex; olfactory tubercle and piriform process)

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2
Q

CN II

A

Optic nerve:
optic nerve –> optic chiasm –> optic tract –> lateral geniculate nucleus of thalamus –> optic radiation to visual cortex

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3
Q

CN III

A

Oculomotor nerve:
exits between crus cerebri from oculomotor and Edinger-Westphal nucleus (superior colliculi level)
Superior orbital fissure
Innervates most muscles of the eye + levetator palpebrae muscle; parasympathetics –> accommodation reflex through edinger-westphal nucleus

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4
Q

CN IV

A

Trochlear nerve:
exits posteriorly beneath inferior colliculi of mid-brain from trochlear nucleus (superior oblique muscle of eye)
Superior orbital fissure
Innervates superior oblique muscle (purely motor)

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5
Q

CN VI

A

Abducens nerve:
exits between pons and medulla oblongata from abducens nucleus (floor of fourth ventricle), lateral rectus muscle
Superior orbital fissure
Innervates lateral rectus muscle

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6
Q

CN V

A

Trigeminal nerve:
biggest CN, attaches to lateral pons
Sensory nucleus: mesencephalic nucleus, chief main nucleus, spinal nucleus
Motor nucleus: pons, floor of 4th ventricle at level of cerebellar peduncles, muscle of mastication innervation
Ophthalmic branch: superior orbital fissure
Maxillary branch: foramen rotundum
Mandibular branch: foramen ovale

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7
Q

What are the roles of Aalhpa, beta, delta and C fibers?

A

Aalpha: proprioception, myelinated
Abeta: touch, myelinated
Adelta: pain, myelinated
C: pain, unmyelinated

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8
Q

CN VII

A

Facial nerve:
Facial motor nucleus: stapedius + muscles of facial expression (stylomastoid foramen)
Nucleus solitarius: sensory (bodies in geniculate ganglia)
Superior salivatory nucleus: parasympathetic fibers (salivation and tears)
Internal auditory meatus (together with CN VIII)

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9
Q

CN VIII

A

Vestibulocochlear nerve:
Cerebello-pontine angle
Vestibulo and cochlear nuclei (lateral to the floor of 4th ventricles, pons)

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10
Q

CN IX

A

Glossopharyngeal nerve:
Root at medulla, lateral to olives
Nucleus ambiguus: motor fibers to stylopharyngeus muscle
Inferior salivatory nucleus: parasymp fibers to parotid gland
Nucleus solitarius: taste from 1/3 of tongue, blood pO2/CO2
Spinal nucleus of trigeminal nerve: pain, temperature and general sensation from inner ear, upper phraynx and posterior 1/3 of tongue

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11
Q

CN X

A

Vagus nerve:
root at medulla, lateral to olives
Nucleus ambiguus: motor fibers to larynx, pharynx and upper oesophagus + parasympathetic input to heart
Sensory fibers:
1. Spinal nucleus of trigeminal nerve: general sensation from phar, lar, oes, ear
2. Nucleus solitarius: chemo and mechano receptors from viscera, some taste
Dorsal nucleus of vagus nerve: parasympathetic fibers to viscera

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12
Q

CN XI

A 
Accessory nerve (motor only):
Cranial root: from nucleus ambiguus, splits from spinal root to join vagus at jugular foramen, innervates muscle of pharynx and larynx
Spinal root (C1-6): enters through foramen magnum, innervates sternocleidomastoid and trapezius muscles
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13
Q

CN XII

A 
Hypoglossal nerve (motor only):
hypoglossal nucleus, innervates intrinsic and extrinsic muscles of the tongue, exits from hypoglossal canal (next to foramen magnum)
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14
Q

What is the neurocranium made of?

A

Calvaria (skull cap), basicranium and intracranial region

8 bones: frontal, ethmoidal, sphenoidal and occipital + temporal and parietal (paired)

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15
Q

What is the viscerocranium made of?

A

Facial bones in anterior part of the cranium
Single: mandible and vomer
Paired: maxillae, inferior nasal conchae, zygomatic, palatine, nasal and lacrimal

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16
Q

Through which structure does the medulla oblongata pass?

A

Foramen magnum

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17
Q

Where is the pterion situated?

A

At the level of the sphenoparietal suture

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18
Q

Which structures sit in each cranial fossa?

A

Anterior: frontal lobe
Middle: temporal lobe
Posterior: occipital lobe

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19
Q

Which cranial nerves pass through the jugular foramen?

A

IX, X, XI

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20
Q

What are the dura and arachnoid mater made of?

A

Dura: collagen fibers
Arachnoid: non-vascular connective tissue

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21
Q

What is the middle meningeal artery and where does it run?

A

largest of three paired arteries supplying the meninges; branch of maxillary artery (terminal branch of external carotid); runs through foramen spinosum; supplies dura mater and calvaria; runs beneath the pterion

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22
Q

Which are the cerebral ventricles?

A

Lateral ventricles (anterior, posterior and inferior horns), interventricular foramen, third ventricle, cerebral aqueduct, lateral aperture (allows CSF to go into subarachnoid space (cisterna magna), central canal

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23
Q

How is CSF re-absorbed into systemic veins?

A

Through arachnoid granulations (into superior sagittal sinus)

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24
Q

In between which two structures does the superior sagittal sinus run?

A

Periosteal and meningeal layers of the dura mater

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25
Q

How much energy does sodium pumping take?

A

60% of brains’ energy

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26
Q

What is the threshold of voltage gated sodium channels?

A

-40 mV

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27
Q

How long is the delay in chemical synapses?

A

0.3-0.5 msec

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28
Q

Which NTs are biogenic amines, amino acids and peptides?

A

Biogenic amines: Ach, NE, E, dopamine, serotonin
Amino acids: glycine, glutamate, aspartate, GABA
Peptides: somatostatin, endorphins, enkephalins, dynorphins, bradykinin, substance P

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29
Q

Where do projection neurons sit in the cortex?

A

Layer 5

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30
Q

How do different CNS cell types originate?

A

Dorsoventral position gives types:
Sensory: BMP –> dorsal
Motor: Shh –> ventral
Cells are born at inner ventricular surface

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31
Q

Which type of migration do CNS cells undergo?

A

Radial and tangential

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32
Q

What is the function of radial glia?

A

In adult: structural scaffold
In development: progenitors are radial glia, guide for migrating neurones
Injured brain: source of astrocytes

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33
Q

What is the function of astrocytes?

A

Homeostatic function: blood vessel/brain interface, linking metabolism to function
Refining signalling: removing excess potassium at nodes. removing NTs, insulating synapse
Brain injury: K+ and H2O absorption –> brain swelling, reactive astrocytes form glial scars –> potential trigger for epilepsy

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34
Q

What is prosopagnosia?

A

Damage to the cortex; you can’t recognise faces

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35
Q

What is the frontoparietal network responsible for?

A

Decision making

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36
Q

Where does information from vision feed into?

A

Dorsal attention: executive control of attention

Ventral attention: recognition of salient features

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37
Q

How is language an example of assymmetry?

A

word form area is on the left side of the brain; pure alexia: when corpus callosum is cut –> inability to read words seen in the left visual field

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38
Q

What are the functions of the spinal cord/hindbrain and midbrain in local circuits?

A

Spinal cord/hindbrain: sensory input - motor output (central pattern generator)
Midbrain: integrates startle responses, eye movements

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39
Q

Which CN are situated in the hindbrain and what is this structure responsible for?

A

V-XII; muscle control and sensation (including hearing for the head)

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40
Q

Which CN are situated in the midbrain and what is this structure responsible for?

A

CN III and IV; motor control of eye movement driven both by visual and auditory cues (superior and inferior colliculi)

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41
Q

What are the functions of the hypothalamus?

A

Integrate autonomic and neuroendocrine system: circadian rhythms, energy metabolism, reproductive behaviour, body temperature, defensive behaviour, blood pressure/electrolytes

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42
Q

Which information relayed to the thalamus is the basal ganglia responsible for, and which structures are part of this?

A

reward; caudate, putamen and globus pallidus in cerebrum + substantia nigra in midbrain

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43
Q

Which structures form the lentiform nucleus and striatum?

A

lentiform nucleus: globus pallidus and putamen

Striatum: putamen and caudate nucleus

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44
Q

Which information relayed to the thalamus is the cerebellum responsible for?

A

Error

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45
Q

What are spina bifida occulta and cystica?

A

Occulta: just vertebral arches missing
Cystica: meningocele (meninges + CSF), meningomyelocele (spinal cord + meninges + CSF)

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46
Q

What are the 5 aspects of somatosensation and where is it mediated?

A

Touch, proprioception, pain, itch, visceral; mediated by dorsal root ganglion neurones or trigeminal nerves

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47
Q

What are the four physiological mechanisms of sensation?

A

transduction; transmission; perception; modulation

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48
Q

How are the A and C neurons characterised?

A

Large: Abeta (fastest: large + myelin –> touch and proprioception), Adelta (smaller + myelin –> temperature and nociception)
Small: C (non-myelinating shwann cells –> T, pain, itch)

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49
Q

What is the receptive field of a sensory neuron?

A

Spatial domain where stimulation excites or inhibits the neuron

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50
Q

What are the 4 types of mechanoreceptors responsible for the sense of touch and their characteristics?

A 
Superficial:
1. Meissener's corpuscle: fast-adapting
2. Merkle disk: slow-adapting
Deep:
1. Pacinian corpuscle: fast-adapting
2. Ruffini ending: slow-adapting
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51
Q

What are the two types of muscle receptors?

A
  1. Muscle spindles: in parallel with muscle fibers, sensitive to length change
  2. Golgi tendon organs: in series with main muscle, sensitive to changes in muscle tension
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52
Q

How is temperature signalled?

A

Cold-sensitive fibers: Adelta (show paradoxical response at high T)
Warm-sensitive fibers: C axons

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53
Q

What are the four different modalities of nociceptors?

A
  1. Thermal: Adelta and some C
  2. Mechanical: Adelta
  3. Polymodal: C fibers (sting)
  4. Silent: only responsive in inflamed tissues
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54
Q

What are the three main divisions of the somatosensory cortex?

A

Primary (S1) and secondary (S2) in post-central gyrus + posterior parietal cortex

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55
Q

How is primary somatosensory cortex S1 subdivided?

A

Brodmann’s areas 3a: deep tissue (muscle stretch receptors);
3b (primarily): skin (SA and RA receptors)
1: skin (RA receptors)
2: deep tissue (pressure and joint position)

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56
Q

How do neurons in broadmann’s areas 3b, 1 and 2 vary in their receptive field size?

A

3b: small

1,2: large

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57
Q

What are reflexes and what are its three steps?

A

Stereotyped involuntary response to stimuli; sensory input, information processing and motor output

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58
Q

What is the difference between autonomic and somatic reflexes?

A

Autonomic: mediated by ANS, smooth muscle, cardiac muscle, glands
Somatic: mediated by somatic nervous system, skeletal muscle

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59
Q

What is an example of monosynaptic reflex?

A
  • single synapse between afferent and efferent neurons
    1. Receptor: muscle spindle
    2. Sensory neurone: Aalpha (myelinated), peripheral nerve, dorsal root glanglion (cell body)
    3. Interpretation centre: spinal cord
    4. alpha motor neurone (myelinated)
    5. Effector: muscle extrafusal fibres (neuromascular junction)
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60
Q

What is the structure of muscle spindles?

A

Central region lacks myofibrils: synapse with tonically active sensory neurons;
Outer regions: synapse with gamma motor neurons

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61
Q

What is the structure of Golgi tendons?

A

At the edges of extrafusal fibers; capsule with collagen fibers and sensory receptors lying in series

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62
Q

What is the function of Golgi tendon in case of excessive load on the muscle?

A

Relaxation of the muscle

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63
Q

What is an example of a simple polysynaptic reflex?

A

Withdrawal reflex

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64
Q

What is reciprocal inhibition?

A

Excitation of one group of muscles and inhibition of their antagonists

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65
Q

What is the cross cord reflex?

A

Opposite limb affected –> effects are reversed

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66
Q

What are examples of intersegmental reflexes?

A

Arm and leg movements

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67
Q

What is the function of Renshaw cells?

A

Recurrent inhibition; collateral from spinal motor neurone onto inhibitory interneurones (regulate spinal motor response)

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68
Q

Which are the pyramidal and extrapyramidal tracts?

A

Pyramidal: corticospinal and corticobulbar (to brain stem motor nuclei)
Extrapyramidal: vestibulospinal, tectospinal, reticulospinal, rubrospinal

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69
Q

What is the function of the vestibulospinal tract?

A

From vestibular nucleus (lateral to 4th ventricle in medulla, CN VIII + cerebellum)

  1. Lateral: ipsilateral, control of balance and posture, innervate antigravity muscles (excites ipsilateral extensor motor neurones, inhibits via interneurones flexor motor neurons)
  2. Medial: bilateral, only neck and shoulder
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70
Q

What is the function of the tectospinal tract?

A

From superior colliculi, coordination of head movements in relation to visual stimuli

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71
Q

What is the function of the reticulospinal tract?

A

Keeps general activation of the brain stem

  1. Medial from pons: increases muscle tone and excites voluntary movement
  2. Lateral from medulla: inhibits muscle tone and inhibits muscle movement
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72
Q

What is the function of the rubrospinal tract?

A

red nucleus —> output from cerebellum; contralateral, fine movements

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73
Q

What is the labyrinthine righting reflex?

A

Supra spinal reflex; vestibular reflex; lean off balance –> stimulation of semicircular canals –> motor response of neck and limbs –> maintainence of upright posture

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74
Q

What is the pathway of visual reflexes?

A

optic nerve –> optic chiasm –> optic tract –> LGN –> pretectal area:

  1. E-W nuclei –> CN III
  2. Superior colliculi –> descending reflex pathways –> spinal motor neurones
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75
Q

What does a weak or absent reflex response indicate?

A
  1. damage of the nerves outside the spinal cord (peripheral neuropathy)
  2. motor neuron disease
  3. myasthenia gravis
  4. myopathy (muscle disease)
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76
Q

What does an exxagerated reflex response indicate?

A
  1. spinal cord damage above the level controlling the hyperactive response
  2. higher CNS damage
    - -> disinhibition
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77
Q

What does an asymmetric reflex response indicate?

A
  1. early onset of progressive disease

2. localised nerve damage eg trauma

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78
Q

How does cerebral palsy relate to reflexes?

A

Failed development of higher control –> retention of primitive reflexes and no inhibition –> random and uncontrolled movement

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79
Q

What is the main reason of synaptic potential decay in synapses where glutamate acts at AMPA Rs?

A

AMPA Rs desensitisation

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80
Q

What is the main reason of synaptic potential decay in cholinergic synapses?

A

Destruction of ACh by cholinesterase

81
Q

What is convergence?

A

Different presynaptic neurons send inputs to a single postsynaptic neuron

82
Q

What are the three types of interneuron inhibition?

A
  1. Feed-forward inhibition
  2. Feed-back inhibition
  3. Recurrent inhibition
83
Q

What is the vascular supply to the brain?

A

Carotid arteries –> vertebral arteries –> Circle of Willis –> pial arteries –> penetrating arteries –> penetrating arterioles –> intracerebral arterioles –> capillaries

84
Q

Which cells form the blood brain barrier?

A

Endothelial cells –> pericytes –> astrocytes

85
Q

What is the function of pericytes?

A

Immune function, traps macromolecules

86
Q

What are peri-vascular sheets and glial limitants?

A

Perivascular sheets: rosette structures formed by endfeet of astrocytes onto capillaries
Glial limitants: projections of astrocytes to form layer just below pia mater

87
Q

What is the molecular composition of adherens junctions and tight junctions?

A

Adherens junctions: VE cadherin, PECAM –> alpha, beta or gamma catenin –> actin filaments
Tight junctions: claudin, occludin and JAMs –> ZO1,2,3 –> actin filaments

88
Q

What are the difference in BBB permeability of morphine, codeine and heroin?

A

Morphine: lipophobic, doesn’t pass BBB
Codeine: formed by adding methyl group to morphine —> crosses BBB
Heroin: hydroxyl groups replaced with acetyl groups —> crosses BBB, metabolised to morphine in the brain and can’t get out —> long lasting effect

89
Q

What are ABC transporters?

A

ATP-binding cassette transporters: active efflux mechanisms, many lipophilic drugs are returned to the blood, ie P-gp transporter, breast cancer resistance protein, multi-drug resistance associated protein

90
Q

What are the two types of endocytosis at BBB?

A
  1. Non-selective: fluid phase –> low level

2. Selective: receptor-mediated transcytosis and adsorptive transcytosis

91
Q

What are the functions of the choroid plexus?

A

Produces CSF, synthesises polypeptides, contributes to regulating brain ISF

92
Q

What is the structure of the choroid plexus?

A

Endothelium –> basal infoldings –> ependymal epithelium

93
Q

How does CSF secretion occur?

A

Vectorial transport of Na+, K+, HCO3- and Cl-
Primary driving force: Na/K ATPase –> promotes secondary active transport of Na/H and Cl/HCO3-
At apical membrane: Na, K, Cl and HCO3 exit through transporters and channels, water follows through aquaporin channels

94
Q

What are the volumes of CSF and brain interstitial fluid?

A

Total CSF: 140 ml

Brain and spinal interstitial fluid: 280 ml

95
Q

What is the pathophysiology of Alzheimer’s disease?

A

Removal process of Amyloid beta through receptor mediated LRP-1 is damaged

96
Q

What are quantitative genetic designs?

A

Used to determine to what extent a phenotype is influenced by genes or the environment, cannot reveal which genes are responsible

97
Q

What are molecular genetic designs?

A

Used to determine which genes are responsible for a phenotype, cannot reveal to what extent a phenotype is influenced by genes or the environment

98
Q

What is epistasis?

A

The interaction of genes that are not alleles

99
Q

What is epigenetics?

A

Changes in gene expression that are not due to changes in DNA sequence but can be heritable and mediate the effect of the environment

100
Q

What is the biological basis of aggression in humans?

A

Orbitofrontal cortex and amygdala, steroid hormones, serotonin, norepinephrine and dopamine

101
Q

What is the relation of behaviour to the biopsychosocial model?

A

Behaviour is part of the “psycho” component of the biopsychosocial model

102
Q

What is behavioural medicine?

A

Study of factors that influence how we:

  1. maintain our health (health promoting behaviour)
  2. prevent illness (health preventive behaviours)
  3. manage illness (illness self-managing behaviours)
103
Q

How do psychological models influence physical health?

A
  1. Direct pathway: psychoneuroimmunology

2. Indirect pathway: behaviour –> physical health

104
Q

What are the two learning theories?

A
  1. Classical conditioning (Pavlov): behaviours acquired through associative learning
  2. Operant conditioning (Skinner): behaviours acquired through reinforcement and punishment
105
Q

What are the 4 details of classical conditioning?

A
  1. Extinction of CR (habituation)
  2. Spontaneous recovery
  3. Generalisation
  4. Discrimination
106
Q

What are positive and negative reinforcement and punishment?

A

Positive reinforcement: adding something valuable and desirable
Negative reinforcement: avoiding something unpleasant
Positive punishment: adding something unpleasant
Negative punishment: removing something valuable or desired

107
Q

What are the 4 details of operant conditioning?

A
  1. Reinforcers differ across individuals
  2. time/duration between behaviour and consequence/reinforcement
  3. Size of reinforcement
  4. Patterns of reinforcement
108
Q

What is social learning?

A

Bandura: behaviours are acquired by observing significant others carrying them out

109
Q

What is the COM-B model?

A

Capability, Opportunities, Motivation –> behaviour

110
Q

Which factors influence our perception of internal and external stimuli?

A
  1. Attention
  2. Information processing system: recognition and knowledge (top-down processing)
  3. Emotion
111
Q

What are the three stages of skill acquisition?

A
  1. Cognitive: mental representation
  2. Associative: development of a motor programme
  3. Autonomous: skill becomes implicit
112
Q

What are assimilation and accommodation?

A

Assimilation: calls a four-legged animal a dog from previous knowledge
Accommodation: learns that not all four-legged animals are dogs, i.e. someone points out that this is a cat

113
Q

What are the differences between declarative and procedural knowledge?

A

Declarative: know that –> episodic memory, personal experience, semantic memory, facts, ideas and concepts –> explicit memory (conscious retrieval)
Procedural: know how –> cognitive/problem solving skills, perceptual skills, motor skills, repetition, classical conditioning –> implicit memory (unconscious retrieval)

114
Q

Which are the three important cognitive processes?

A
  1. Perception
  2. Attention
  3. Additional information processing
115
Q

What are the three types of health behaviour?

A
  1. Risky
  2. Promotive/protecting
  3. Illness-related
116
Q

What are the 5 determinants of health behaviour?

A
  1. Social factors
  2. Reinforcement value
  3. Symptoms
  4. Emotional factors
  5. Cognitive factors (beliefs and attitudes)
117
Q

What is the health belief model?

A

Likelihood of behaviour change depends on:

  1. perceived threat: perceived susceptibility + perceived severity
  2. cost benefit assessment: perceived cost/barriers + perceived benefits
118
Q

According to the HBM, which factor is most important in preventing change?

A

Perceived barriers

119
Q

What is the theory of planned behaviour?

A

Behavioural intention drives behaviour and depends on:

  1. Attitude towards behaviour
  2. Subjective norm
  3. Perceived behavioural control
120
Q

What are implementation intentions?

A

Bridge the intention-behaviour gap; combine intention to behaviour with clear plan of action

121
Q

What is self-efficacy?

A

Belief/confidence that one can perform a behaviour

122
Q

What is evidence based medicine?

A

Integrating individual clinical experience with the best available clinical evidence from systematic research

123
Q

What are the stages of motivational interviewing?

A
  1. Engagement
  2. Focussing
  3. Evoking
  4. Planning
124
Q

What are the four guiding principles of motivational interviewing?

A
  1. Expressing empathy
  2. Supporting self-efficacy
  3. Rolling with resistance
  4. Develop discrepancy
125
Q

What are the 4 skills in motivational interviewing?

A

OARS:

  1. Open questions
  2. Affirm
  3. Reflect
  4. Summarise
126
Q

How are you able to evoke change talk?

A

DARN:

  1. Desire
  2. Ability
  3. Reason
  4. Need
127
Q

What are the importance and confidence rulers?

A

Importance ruler: from 0-10 how important do you feel is to walk regularly?
Confidence ruler: from 0-10 how confident do you feel that you will achieve your goal?

128
Q

What are the BCTs recommended by NICE?

A

Goal setting and planning, feedback and monitoring, social support, “if-then” planning

129
Q

What can symptoms be attributed to?

A

somatic causes, psychological causes or environmental

130
Q

What are the psychological factors that can explain variation in symptom reporting and healthcare utilisation?

A
  1. Attention
  2. Attribution
  3. Emotions
131
Q

What are the reasons for delays in help seeking?

A
  1. Appraisal delay
  2. Illness delay
  3. Utilisation delay
132
Q

What is the common sense self-regulatory model (CS-SRM) of illness?

A

Emphasis on personal, common-sense beliefs about illness, based on illness schema

  1. Illness perceptions –> coping behaviour –> appraisal of illness representation and coping behaviour
  2. Emotional response –> coping behaviour –> appraisal
133
Q

What are the 5 key determinants of patients’ illness perceptions?

A
  1. Identity
  2. Cause
  3. Timeline
  4. Consequences
  5. Cure and control
134
Q

What is coping?

A

General term to describe the different cognitive and behavioural efforts used by patients to deal with demands of illness

135
Q

What are the two main coping styles?

A

Problem-focused: dealing directly with demands by active involvement
Emotion-focused: dealing with anxiety, uncertainty and other negative emotions (by distraction, avoidance or expression), re-frame illness in a positive light, utilise social support

136
Q

When do you use problem-focused coping and when emotional-focused coping?

A

Emotional-focused: little control

Problem-focused: greater control

137
Q

What are unintentional and intentional non-adherence?

A

Unintentional non-adherence: capacity/functional limitations + resource limitations
Intentional non-adherence: making a decision not to take all of the doses as prescribed (motivation, illness perceptions, treatment perceptions)

138
Q

What are the 2 determinants of patients’ treatment perception?

A
  1. Necessity

2. Concerns

139
Q

What are the strongest predictors of adherence?

A

Treatment beliefs: high necessity, low concerns

140
Q

How are treatment beliefs and risk of non-adherence connected?

A
  1. High concerns and low necessity –> skeptical (high risk)
  2. High concerns and high necessity –> ambivalent (medium risk)
  3. Low concerns and low necessity –> indifferent (medium risk)
  4. Low concerns and high necessity –> accepting (low risk)
141
Q

How do you improve adherence?

A
  1. Removing barriers (unintentional)
  2. Improving communication (knowledge, memory, instruction)
  3. Identifying maladaptive illness and treatment perceptions and modifying them (intentional)
142
Q

How does the HPA axis work in stress?

A

Stimulus (stressor, expectations, emotions) –> amygdala releases CRF –> hypothalamus releases CRF –> pituitary secretes ACTH –> adrenal cortex secretes cortisol –> acts on glucocorticoid receptors in hippocampus, prefrontal cortex, hypothalamus and pituitary
*In acute stress, negative feedback from PFC and hippocampus –> less release of CRF and ACTH

143
Q

What is the difference between affective and anxiety disorders?

A

Affective disorders: low mood, unhappiness, sadness (major depression, manic-depressive illness, bipolar depression, post-natal depression)
Anxiety disorders: fearfulness, apprehension or anxiety (generalised anxiety disorder, panic disorder, phobias, OCD)

144
Q

What is schizophrenia?

A

Positive symptoms: hypersensitivity and hyperawareness of thoughts and cognitive functions; some may experience auditory or visual hallucinations, others paranoia or anxiety or delusional thoughts; psychosis is at the root of all symptoms: inability to distinguish between real and unreal perceptions
Negative symptoms: loss of normal mental function, lack of emotions and loss of motivation

145
Q

What is dysthymia?

A

A few mild but persistent symptoms leading to a persistent low grade depression

146
Q

What are the mechanisms of action of antidepressants?

A

Inhibition of presynaptic and extra-synaptic uptake (TCAs, SSRIs, NSRIs, SNRIs)

147
Q

What are the treatments available for mild, more severe and very severe depression?

A

Mild: cognitive psychotherapy
More severe: psychotherapy + drug therapy or drug therapy alone
Very severe: electroconvulsive therapy (ECT)

148
Q

What are the two ascending pain pathways?

A

Spinothalamic: discriminative aspect of nociception (fast pain), contralateral
Spinoreticular: responsible for arousal and unpleasant sensations (dull pain), contralateral

149
Q

Where do sensory neurons in the spinal cord terminate?

A

Laminae I and II

150
Q

What is the descending pathway modulating pain?

A

Periaqueductal grey matter –> rostro ventromedial medulla (RVM; nucleus raphe magnus) –> spinal cord

151
Q

Which factors regulate the gate in the gate control theory of pain?

A
  1. Amount of activity pain fibers
  2. Amount of activity in peripheral pain fibers (mechanoreceptor activation of Abeta)
  3. Messages descending from brain
152
Q

What are the three components of the subjective experience of pain?

A
  1. sensory-discriminative
  2. affective-motivational
  3. cognitive component
153
Q

What are the different types of pain?

A

Adaptive: nociceptive and inflammatory

Maladaptive (pathaological): neurpathic and dysfunctional

154
Q

What are allodynia and hyperalgesia?

A

Allodynia: thersholds are lowered so that stimuli that would normally not produce any pain now begin to
Hyperalgesia: responsiveness is increased, so that noxious stimuli produce an exaggerated and prolonged pain

155
Q

What are the mechanisms involved in pain hypersensitivity?

A
  1. Peripheral sensitisation: due to action of inflammatory chemicals
  2. Central sensitisation: increase in the excitability of neurons within CNS, triggered by a burst of activity in nociceptors which alter the strength of synaptic connections btw nociceptors and spinal cord neurons
156
Q

What are the stages of child development?

A 
Infancy (0-2): attachment, maturation of sensory, perceptual and motor functions and understand objects through senses
Early childhood (2-6): locomotion, fantasy play, language development, sex role identification and group play
Middle childhood (6-12): friendship, skill learning, self-evaluation, team play, understand cause and effect and conservation
Adolescence (12-18): physical maturation, emotional development, peer group and sexual relationships, understand abstract thinking
157
Q

What are the critical periods for sitting without support, standing with assistance, hands and knees crawling, walking with assistance, standing alone, walking alone?

A 
sitting without support: 4-9 months
standing with assistance: 5-11.5 months
hands and knees crawling: 5-13.5 months
walking with assistance: 6-14 months
standing alone: 7-17 months
walking alone: 8.5-17.5 months
158
Q

What is perceptual development?

A

Babies are able to fixate their gaze, focus on areas of contrast, active information seeking, development appropriate selective attention (6 years)

159
Q

What are the 5 stages of language development?

A
  1. Preverbal communication
  2. Phonological development
  3. Semantic development
  4. Syntax and grammar development
  5. Pragmatics development
    * first words at approximately 1 year
160
Q

How does words learning evolve in development?

A 
9-13 months: first words
12-18: 3 words a month
18 months: know 22 words
"naming explosion: 10-20 words per week
Age 6: 10000 words, five new words a day
161
Q

What are the 4 key concepts of Piaget’s theory on developing cognitive skills?

A
  1. Schema: internal cognitive structure which provides procedure to use in specific circumstances
  2. Assimilation: process of using schema to make sense of event or experience
  3. Accomodation: changing schema as a result of new information
  4. Equilibration: process of balancing assimilation and accommodation to create schemes that fit the environment
162
Q

What are the 4 key stages of Piaget’s theory on developing cognitive skills?

A

Stage 1 Sensorimotor (0-2 years): initial reflexes, child interacts with the environment and manipulates objects, understanding of object permanence
Stage 2 Preoperational (2-6/7): internal representation of concrete objects and situations, child uses symbolic schemes like language, egocentric, reasoning dominated by perception
Stage 3 Concrete Operations (6/7-11/12): reasoning involves more than one salient feature (conservation), logical reasoning can only be applied to objects that are real or can be seen, no longer egocentric, understand principles of conservation
Stage 4 Formal Operations (11/12+): can think logically about potential events or abstract ideas, can test hypotheses about hypothetical events

163
Q

What is the timeline of social development in children?

A

1st few months: specificity towards caregiver
8 months: separation anxiety and fear of stranger
10 months: social referencing
Attachment: 6 months - 2 years (critical period)

164
Q

What are the 4 attachment styles described in Bowlby’s theory of attachment?

A

Type A: insecure, anxious, avoidant –> carer who is rejecting
Type B: secure –> carer who is available, sensitive and supportive
Type C: insecure, anxious/resistant –> carer who is inconsistent
Type D: insecure, disorganised –> carer who is inconsistent and may abuse the child

165
Q

What is primary and secondary ageing?

A

Primary ageing: expected changes - largely biologically determined and intrinsic to ageing process (speed of processing, wrinkles, grey hair)
Secondary ageing: changes influenced by behaviour

166
Q

What are ADL and IADL?

A

Activities of daily living and instrumental activities of daily living

167
Q

What are the 3 components to successful ageing?

A
  1. Good physical health
  2. Retention of cognitive abilities
  3. continuing engagement in activities: social support and productive activity
168
Q

What are the three steps for adaptive process to attain valued goals?

A

Selection, optimisation and compensation

169
Q

What is the post fall syndrome?

A

Fall –> fear of falling again –> less exercise –> decreased muscle strength and balance –> increased risk of falling

170
Q

What are the three stages of dementia?

A

Mild: judgement retained but effects on memory, work and social activities
Moderate: independent living becomes difficult, mini mental state examinations and word lists
Severe: severe impairment with all ADLs and needs constant supervision

171
Q

What is the internal capsule and where is it situated?

A

Band of white matter in cerebral hemispheres through which almost all tracts enter or leave the cerebral cortex; between lentiform nucleus (globus pallidus and putamen) laterally and thalamus and head of caudate nucleus medially; divided into: anterior limb, genu, posterior limb and retrolenticular part

172
Q

What is the function and structure of the thalamus?

A

23 nuclei; anterior, medial and lateral regions separated by Y shaped band of axons (laminae); gateway to the cerebral cortex for all sensory inputs apart from olfactory pathway; spinal cord input: ventro-posterior nucleus (VP), lateral part (VPL); trigeminal input from face: medial part of VP (VPM)

173
Q

Where are the primary motor cortex and somatosensory cortex situated?

A

Primary motor cortex: pre-central gyrus

Somatosensory cortex: post-central gyrus

174
Q

What are the causes of spastic vs flaccid paralysis?

A

Spastic: neurons in the brain and spinal cord that activate the motor neuron
Flaccid paralysis: spinal and cranial motor neuron that directly innervate the muscle

175
Q

What is Durkheim’s proposed explanation for suicide?

A

Influenced by: level of social integration and level of social regulation

176
Q

What are the four categories of suicide according to Durkheim?

A

Egoistic: insufficient social integration, insufficient social bonds
Altruistic: excessive social integration, individual less important than society
Anomic: insufficient regulation, state of anomie caused by major social, economic change
Fatalistic: excessive regulation (prison)

177
Q

What is the reward pathway and what is the action of alcohol on this pathway?

A

Mesocorticolimbic pathway: dopaminergic pathway involved in reward; alcohol enhances release of dopamine by quieting neurons that inhibit dopamine secretion; pathway: substantia nigra + ventral tegmental area –> striatum, nucleus accumbens, cingulate gyrus and prefrontal cortex

178
Q

What are the genetic effects of alcoholism?

A

A1 allele on D2 receptor –> reduced number of dopamine binding sites and increased likelihood to develop substance abuse
RASGRF-2 variation –> higher sense of reward with alcohol use

179
Q

What are orexins?

A

Neuropeptides synthesised in the hypothalamus and modulating many NT systems; involved in feeding behaviour, neuroendocrine regulation, sleep-wake cycle and reward-seeking; orexin blockers can make rats stop drinking freely available alcohol

180
Q

How did Popper define the nature of science?

A

A scientific statement is one that is in principle refutable

181
Q

Why is it important for social scientists to focus on induction?

A
  1. Research question is not necessarily about causes, but may be about: reasons, mechanisms and context
  2. A natural object such as a molecule does not react to the process of being observed, but people do
182
Q

When are qualitative methods more and less appropriate?

A

More appropriate: exploring a new area where little is known, generate new hypotheses, understand patient perspectives in detail, understand process of change
Less appropriate: answer a question about causation, quantify something (how many patients, how much improvement)

183
Q

What is the clinical importance of the cavernous sinus?

A

passage of internal carotid –> break –> obstruction of CNIII, IV, VI and V (ophthalmic branch)

184
Q

What is trigeminal neuralgia?

A

caused by: compression of blood vessels, herpes infection, tooth or jaw infection, brain stem tumour, demyelination

185
Q

What does accessory nerve injury lead to?

A

winging scapula

186
Q

What does compression of CN IX-XII by tumours lead to?

A

Dysphonia, unilateral weakness, wasting and fasciculation of the tongue, suppression of gag reflex, unilateral wasting of sternocleidomastoid and trapezius, changed taste sensation

187
Q

What is motor neuron disease and what does it lead to?

A

Chronic degenerative disorder, degeneration of corticobulbar tracts, nucleus ambiguus and hypoglossal nucleus –> dysphonia, dysphagia, dysarthria, weakness and spasticity of the tongue

188
Q

What is retinitis pigmentosa?

A

mutation in rhodopsin gene –> blindness

189
Q

How does rhodopsin work?

A

dark –> inactive rhodopsin –> open Na+ channels –> depolarisation –> glutamate release –> bipolar cell either activated or inhibited depending on glutamate receptor

190
Q

How does sensory transduction in hearing work?

A

endolymph surrounds stereocilia; opening of channels leads to K+ influx into hair cell –> depolarisation –> opening of Ca2+ channels –> release of vesicles filled with excitatory NTs

191
Q

How many different odorant receptors are there?

A

100-200

192
Q

How is hearing coded?

A

position in the cochlea; higher frequencies at base, lower frequencies at apex

193
Q

What is illness behaviour?

A

The ways in which given symptoms may be differently perceived, evaluated and acted upon by different kinds of people

194
Q

Which factors determine illness behaviour?

A
  1. propensity to seek the sick role
  2. social triggers
  3. decision-making models (health beliefs model)
  4. an interpretive model
195
Q

What does temporalizing mean?

A

Saying I’ll go to the doctor if my chest pain worsens

196
Q

What is the interpretive model?

A

People try to make sense of their conditions and when they fail they go to see the doctor

197
Q

What is Stewart and Roter’s model of degrees of control?

A

Doctor and patient control low –> default
High doctor control and low patient control –> paternalism
Low doctor control and high patient control –> consumerism
High doctor and patient control –> mutuality

198
Q

What is compliance?

A

The extent to which the patient’s behaviours matches the prescriber’s recommendation, implies lack of patient involvement

Genes and Behaviour (4 decks)

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