Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Module 202 > CSA 2 > Flashcards

CSA 2 Flashcards

1
Q

What is pain?

A

Unpleasant sensory experience associated with tissue damage, accompanied with an emotional response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why do we feel pain?

A

Warning sign– avoid harmful situations, prevent further injury or death, signal to rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the possible categories of sensations of pain?

A

Sharp stab, throbbing, burning, deep ache, freezing, Itch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 classifications of pain?

A

Nociceptive (normal functioning of nociceptors), Inflammatory (pain in response to inflammation), Neuropathic (in response to injury to nervous system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are nociceptors?

A

Primary sensory neurons that detect pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the classifications of afferent nerve fibres? Describe nerve structure, use, and conduction speed.

A

A-alpha and A-beta (myelinated, large diameter, light touch, proprioception 30-75 m/s), A-delta (thinly myelinated, medium diameter, light touch, temperature, nociception, 5-30 m/s), and C fibres (unmyelinated, small diameter, temperature, nociception 0.5-2 m/s).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is special about nociceptors in the periphery?

A

They have free nerve endings.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name 4 types of specialised A-Beta fibres and uses.

A

Meissner’s (stroke/fluttering), Pacinian (vibration), Merkel discs (pressure), Ruffini (Stretch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What kind of pain do c fibres produce? Describe pain transduction.

A

Slow dull ache, burning pain, poorly localised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What kind of pain do Adelta fibres produce? Describe pain transduction.

A

sharp pricking pain, well localised, acitvation of reflex arcs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the significance of having polymodal nociceptors?

A

Pain can result from pressure, temperature, and chemical responses, distinguished in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Discuss Pressure Transduction Mechanism

A

Not yet identified in eukaryotic cells, mechanosensitive channels (Potentially acid sensing channels, or transient receptor potential TRP channels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Discuss Temperature Transduction Mechanism

A

via TRP channels, TRPV1 (transience receptor potential vannilloid 1) used for Hot or capsacin. TRM for cold/menthol. TRPA1 for very cold or cinammon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe pain pathway among first order neurons

A

Spinothalamic tract: Enter dorsal horn, form tract of lissauer, synapse in substantia gelatinosa, glutamate and substance p excites second order neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe pain pathway among second order neurons

A

Cross in dorsal horn at each level, ascend in anterolateral column to thalamus, synapse on third order neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes referred pain?

A

Convergence of visceral and cutaneous nociceptors on same second order neurons in spinal cord. Brain perceives this as cutaneous pain (eg angina perceived in upper chest wall and left arm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe pain pathway among third order neurons

A

Ascend to primary somatosensory cortex (lower body to medial cortex, upper body to lateral cortex). Project to insula and cingulate cortex to encode emotional components of pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why do some battle victims report no pain?

A

Stress-induced analgesia, activated by higher cortical pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two important areas of descending regulation of pain? Describe path and purpose.

A

Periaqueductal gray matter (PAG) and Raphe Nucleus Magnus (in rostral ventromedial medulla). PAG to Raphe Nucleus to dorsal horn, modulates activity of spinothalamic tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can the Raphe nucleus inhibit the spinothalamic tract?

A

Serotonergic projections excite inhibitory interneurons, which inhibit second order spinothalamic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do opioids inhibit pain?

A

Act on inhibitory metabotropic receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where are opioids released?

A

From interneurons, multiple sites: midbrain (PAG), medulla (raphe nucleus), dorsal horn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What activates nociceptors?

A

ATP (purinergic receptors P2X), H+ (acid sensing ion channels), Serotonin (5HT3 receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does the activation of one branch of a nociceptor axon trigger?

A

Release substance p and CGRP from another, causing vasodilation, increased permeability, activation of mast cells (releasing histamine = more inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What impact does inflammation have on pain?

A

Pain hypersensitivy, feels more painful!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name the two types of pain hypersensitivity

A

allodynia- non-noxious stimuli produce pain, hyperalgesia- noxious stimuli produce exaggerated response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the mechanisms of pain hypersensitivity?

A

peripheral sensitization in primary hyperalgesia, and central sensitization in allodynia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What makes peripheral ends of nociceptors more sensitive?

A

Bradykinin and NGF reduce threshold of heat activated channels (bind to TRPV1 receptor, activates protein kinase which phosphorylates TRPV1), prostaglandin reduces threshold of sodium channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is pain categorised by time?

A

Less than 3 months acute, more is chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name one type of local anaesthetic and describe its mechanism of action

A

Lidocaine, lignocaine, topically applied, sodium channel blocker (prevent nociceptor firing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are NSAIDs? Give two examples explain and how they work.

A

Non-steroidal ant-inflammatory drugs (aspirin, ibuprofen), reduce inflammatory response by inhibiting prostaglandin synthesis, preventing peripheral sensitization. cyclooxeganase (COX) inhibited= prostaglandind synthesis reduced = prevented decrease in NA+ channel threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does paracetamol work?

A

NOT NSAID. Acts centrally: inhibits COX enzymes in CNS, acts on descending serotonergic pathways, exact mechanism unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why is capsaicin cream useful?

A

TRPV1 channel agonist, repeated application causes peripheral terminals to die back (calcium overload = mitochondrial dysfunction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the idea of modulating pain at the level of the spinal cord called? Describe how this might work.

A

Gate control theory: pain evoked by nociceptors can be reduced by simultaneous activation of low threshold mechanoreceptors (A-beta fibres). eg rubbing/blowing on painful area to reduce pain sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does stimulating A-Beta fibres do to activated c fibres?

A

activates interneurons in dorsal horn, which inhibit spinothalamic neurons (including c fibres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the mechanism of action of opioids.

A

Agonists of the endogenous opioid system. Sites of action in brain stem (disinhibition), spinal cord, and periphery (inhibit channels on nociceptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Name 6 mechanisms that could cause neuropathic pain.

A

compression, traction, sever, hypoxia, demyelination, tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How much of the population suffers from neuropathic pain?

A

~8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe a neuroma and its implication.

A

At injury site, a neuronal axon will grow many small sprouts, meaning many more ion channels, leading to a more excitable axon (can lead to phantom limb pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the two central mechanisms of neuropathic pain?

A

central sensitization and cortical remapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the underlying mechanisms of central sensitization?

A

reduced threshold for activation of 2nd order neurons, synaptic reorganisation, reduced inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the steps leading to reduced threshold for activation of the CNS?

A

long-term potentiation: constant firing of axons from periphery following injury, sustained release of glutamate, prolonged depolarisation of post synaptic membrane, massive influx of Ca2+, activation of kinases, phosphorylation of NMDA/AMPA receptors, phenotype change leading to more ion channel production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens after central sensitization?

A

A-Beta fibres synapse onto 2nd order spinothalamic neurons, normally non-functional but now activated, leading to allodynia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What happens in synaptic reorganisation?

A

A-Beta fibres form new sprouts that synapse onto spinothalamic tract neurons, causing allodynia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is important to know about treating chronic pain patients.

A

Acute tx does not work– need individual plans, especially management of primary condition and other associated symptoms. 80% are depressed. Sleep disturbances, fatigue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What drugs help with chronic pain?

A

Tricyclic antidepressants, anticonvulsants, NMDA antagonists,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What non-drug treatments help with chronic pain?

A

Physiotherapy, psychological therapies, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name a tricyclic antidepressant and its MOA

A

Amitryptyline, unclear MOA, act on descending inhibitory pathways, inhibits reuptake of serotonin (SSRI activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name two anticonvulsants and their MOA

A

Gabapentin (and pregabalin) and carbamazepine. MOA unclear, act in spinal cord to reduce excitability, blocks calcium (gabapentin) and sodium (carbomazepine) channels. Gabapentin does NOT work on GABAergic interneurons, blocks presynaptic voltage-gated Ca2+ channels, prevents release of glutamate from nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Name one NMDA antagonist and describe mechanism of action.

A

Ketamine, NMDA receptor antagonist reduces glutamate influx, prevents depolarization of second order neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the first, second and third line tx for neuropathic pain?

A

Amitriptyline or pregabalin, then switch or combine, then refer to pain specialist and consider oral opioid or topical lidocaine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What non-drug treatments are there for neuropathic pain?

A

placebo, acupuncture, massage therapy, homeopathy, herbal medicine, hypnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the anatomical features of the basal ganglia?

A

Gray matter nuclei deep within the brain, most superior is caudate nucleus split into head and tail (cat’s tail), lateral and inferior to caudate is putamen, lateral and deep to putamen is globus pallidus, thalamus is posterior (technically separate but has key interactions w basal ganglia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the two structures related to the basal ganglia located underneath the thalamus?

A

subthalamic nucleus and substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the pallidum?

A

internal and external global pallidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the putamen and globus pallidus called?

A

lentiform nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the caudate + putamen + pallidum?

A

Corpus striatum, white matter of ascending and descending tracts, divided by internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the caudate + putamen?

A

neostriatum (caudate = dorsal striatum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is one of the roles of the basal ganglia?

A

interface with cortex to filter movement options

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are 3 other pathways of the basal ganglia besides motor coordination?

A

oculomotor loop: coordinates eye movement, prefrontal loop: executive functions eg working memory, limbic loop: reward processing/behaviour, related to addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe the direct pathway of the basal ganglia.

A

Cortex to Striatum to Globus Pallidus Internal to Thalamus back to cortex. Double inhibition link, GPi inhibits thalamus but can be inhibited by striatum. Allows movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe the indirect pathway of the basal ganglia.

A

Prevents movement. Cortex to striatum to Globus Pallidus External to Subthalamic nucleus to Globus Pallidus Internal to thalamus back to cortex. Double inhibition before and after GPe (inhibits STN but inhibited by striatum) .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the hyperdirect pathway of the basal ganglia.

A

Emergency stop. Cortex to subthalamic nucleus to globus pallidus internal to thalamus back to cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does striatum know if a motor plan is to be promoted or prevented?

A

2 populations of striatum, Direct D1 and Indirect D2. D1 receptor activates by dopamine, D2 dampened down by dopamine release. Dopamine promotes movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what releases dopamine?

A

substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is dopamine activity/release to basal ganglia opposed?

A

Acetylcholine opposes dopamine, dampens D1 direct pathway, activates indirect D2 pathway. Ach prevents movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is characterised by a high amplitude unilateral flailing of the limbs? Describe the pathway and cause.

A

Ballismus, hemiballismus if one half the body. Defect in subthalamic nucleus in indirect pathway, leading to greater excitation in thalamus, caused by stroke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are tic disorders and how are they categorised (4)?

A

Brief repetitive stereotypes movements with a premonitary urge. Simple (blinking, coughing), Complex (jumping, twirling), Plus (motor disorder), Coprolalia (swearing - rare)

69
Q

What makes tic disorders better or worse?

A

Reduced by distraction, concentration. Worsened with anxiety or fatigue.

70
Q

What are tic disorders associated with?

A

50% have adhd, 33.3% have ocd, up to 50% have anxiety, complex genetic inheritence, post infectious immune

71
Q

What are jerky, brief, irregular contractions that are not repetitive or rhythmic but appear to flow from one muscle to the next?

A

Chorea, patient appears fidgety, restless.

72
Q

What are the genetic features of Huntington’s chorea genetics?

A

Trinucleotide repeat on chromosome 4. Autosomal dominant with complete penetrance, the longer the repeat sequence the earlier the onset

73
Q

How does Huntington’s present?

A

cognitive (undecisive, unable to multitask, slowness of thought), Behavioural (irritability, depression, apathy, anxiety, delusions), Physical (chorea, motor persistence, dystonia, eye movements)

74
Q

What are brief jerks with rapid onset and offset?

A

myoclonus

75
Q

What is the pathophysiology of myoclonus?

A

unknown, possibly imbalance between inhibitory and excitatory neurotransmitters (explains why treatable with antiepileptics), perturbations of motor control system leading to a brief disequilibrium (explain why present at multiple levels)

76
Q

What are the causes of myoclonus?

A

Juvenile myoclonic epilepsy, brain hypoxia, prion disease

77
Q

What is implicated in abnormal twisting posture- often axial/facial.truncal, may also have jerky tremor

A

dystonia

78
Q

What is the pathophysiology of dystonia?

A

Not fully understood, fPET suggests abnormal activity in motor cortex, supplementary motor areas, cerebellum, basal ganglia. Abnormal dopaminergic activity in basal ganglia suggested by dystonia being cause by blocking dopamine receptors, some dystonias being levodopa responsive.

79
Q

What causes dystonia?

A

Stroke, brain injury, encephalitis, parkinson’s, huntington’s

80
Q

What drugs are administered in patients with hyperkinetic disorders?

A

Dopamine D2 receptor blocking agents, dopamine depleting agents, atypical anti-psychotics

81
Q

What adverse events are most often seen in dopamine blocking drugs?

A

Acute: oculogyric crisis, neuroleptic malignant syndrome. Subacute: drug induced parkinsonism. Long term: dyskinesias

82
Q

What triad of symptoms described hypokinetic disorders (parkinsonism)?

A

Slowness of movement, stiffness, shaking (rest tremor)

83
Q

What non-motor symptoms are associated with parkinson’s?

A

Depression, anxiety, dementia, sleep disturbance (restless legs, REM parasomnia), reduced sense of smell, autonomic involvement (postural hypotension)

84
Q

what part of the pathway is damaged in parkinson’s?

A

substantia nigra: less dopamine release leads to increased activity of the indirect pathway leads to less movement

85
Q

What can cause parkinson’s disease?

A

Neurodegenerative >80% (diffuse lewy body disease, atypical parkinsonism), drugs that block dopamine, hydrocephalus, metal toxicity, Genetic (metabolic- wilson’s disease)

86
Q

What is the treatment for parkinson’s?

A

L-Dopa gold standard to increase dopamine, anticholinergics (remove Ach which opposes dopamine), MAOI-type B (type A interacts with common foods cheese, red wine, etc) to prevent breakdown

87
Q

What are the ways to increase dopamine?

A

Increase levodopa to produce it, or decrease COMT or MAOB to stop breakdown, decrease Ach

88
Q

What must you remember when administering L-Dopa?

A

Always combine with dopa decarboxylase inhibitor to prevent peripheral conversion to dopamine

89
Q

What systems and pathway do drugs hijack?

A

Mesolimbic and Mesocortical systems = Mesocorticolimbic pathway (reward & reinforcement, motivation). Also pre-frontal cortex, nucleus accumbens, amygdala, and hippocampus.

90
Q

What is the pathway for pleasure?

A

Ventral tegmentum area to Nucleus accumbens to pre-frontal cortex

91
Q

What is the difference between tolerance and dependence?

A

Tolerance the the diminishing effect of a drug after repeated use, more is needed to achieve the same outcome. Dependence is an adaptive state, the physical or emotional homeostatic response to repeated drug administration, unmasked by withdrawal.

92
Q

What receptors do opiates and benzodiazepenes work on?

A

Opioid receptors for opioids and GABA receptors for benzos

93
Q

Describe the rat experiment on addiction.

A

A rat will continuously press a lever that stimulates the medial forebrain bundle (MFB, includes mesolimbic path from ventral tegmentum area to nucleus accumbens) until it is exhausted.

94
Q

How does the reinforcement system work, generally and in addiction?

A

Recognise something good has happened, strengthen neural connections between neurons that detect the stimulus and those producing the instrumental response… long-term potentiation. In addiction, potential sites = glutamatergic synapses on reciprocal connections between

95
Q

What is the connection between memory and relapse?

A

Higher chance of relapse in areas connected to drug use by memory (eg night club and cocaine)

96
Q

What is the effect of dopamine on long term potentiation? How does this happen?

A

dopamine enhances LTP. At D1 receptors, modifies transmission of glutamate allowing LTP. Memories in these pathways may trigger relapse years later.

97
Q

What is the mechanism by which cocaine and amphetamines increase dopamine?

A

Cocaine inhibits dopamine reuptake transporter. Amphetamine increases the amount of dopamine release.

98
Q

How does the brain respond to the long-term increase in dopamine provided by cocaine or amphetamine?

A

Decreases DA transporters and terminals to compensate, hypofrontality, cellular and molecular changes that promote dysregulation

99
Q

What is experienced during withdrawal when there is emotional dependence? What is responsible for this?

A

Anhedonia, dysphoria, anxiety. Dynorphin released in VTA is responsible.

100
Q

What opioids are replacement therapies for other opioids?

A

Methadone (mu-opioid receptor agonist, half life 8-59 hours, full effect 3-5 days) and buprenorphine (partial `agonist at opioid receptors, antagonist at kappa opioid receptors, half life 37 hours)

101
Q

What area of the brain controls attention, vigilance, and arousal (as well as the fight or flight response)?

A

Locus Coerules

102
Q

What neurotransmitter does alcohol and amphetamine dependence work on?

A

GABA only, (activates GABA receptors and inhibits NMDA, brain downregulates net inhibitory effects). Alc and benzos stop = loss of inhibition = firing to point of seizure (general tonic clonic)

103
Q

How long does alcohol withdrawal last for 10-15 units?

A

6 Days for minor withdrawal syndrome, Wernicke’s encephalopathy (thiamine B1 deficiency) on day 9

104
Q

What neurotransmitters does MDMA work on and what does it do to them?

A

Increases noradrenaline, 5-HT, Dopamine

105
Q

What is the downside to repeated MDMA use?

A

Long-term serotonin depletion from Raphe Nucleus

106
Q

What is the mechanism of action of ketamine?

A

Reduces excitatory action at NMDA receptors, results in dissociation. Long-term use results in ketamine bladder.

107
Q

What is used to detox from alcohol?

A

Chlordiazepoxide or other benzodizepines

108
Q

What is the most important thing to keep in mind when selecting a benzo?

A

half life

109
Q

What drugs are used to help maintain alcohol abstinence and what are there MOAs?

A

Acamprosate (MOA unclear, effects on NMDA?), Naltrexone (opiate antagonist, reduces alc euphoric effect), Disulfram (aversive, become unwell)

110
Q

What drugs are used to help maintain opiate abstinence and what are there MOAs?

A

Naltrexone, opiate antagonist, opiates cannot bind to receptor and have no effect. Or long-term stabilisers.

111
Q

What is priming?

A

Tiny ‘taste’ of a drug leads to wanting more

112
Q

What is an emotion?

A

Transient event, produced in response to external or internal events of significance to the individual, characterised by attention to the evoking stimulus and changes in physiological arousal, motor behaviour, and feelings and engender a biasing of behaviour.

113
Q

How many emotions are there and what are they?

A

6 basic by Ekman: Anger, Fear, Disgust, Surprise, Happy, Sad.

114
Q

What is an alternative basic set of emotions?

A

8 basic: joy + sadness. Trust + disgust. Fear + anger. Surprise + anticipation. Can be blended.

115
Q

Who created different classifications of emotions and what were they?

A

Ekman: studies of facial expressions across cultures. Frijda: class emotions by predisposition to actions.

116
Q

How are physiological states integrated into awareness?

A

Thalamus projects to Insula, which appears to encode physiological information.

117
Q

What is the James-Lange theory of emotion?

A

Perceive a stimulus, followed by physiological changes. After event, emotion is “felt.”

118
Q

What is the Cannon-bard theory of emotion?

A

Perceive a stimulus, followed by emotion, followed by physiological changes which guide behaviour.

119
Q

What is the Schacter and Singer experiment on emotion and what did it show?

A

Three groups given adrenaline (informed, misinformed, ignorant) and exposed to euphoric or anger conditions. Least susceptible were informed because they understood why they felt as they did.

120
Q

What can down-regulate emotions?

A

Dorsolateral Pre-Frontal Cortex can dampen emotional responses.

121
Q

What is the difference between psychosis and neurosis?

A

Psychosis is categorised by loss of boundaries with reality and loss of insight with primary features of delusions and hallucinations. Includes schizophrenia, bipolar disorder, depressive psychosis. Neurotic pt is in touch w reality, has anxiety disorders, depressive disorders, OCD, adjustment disorders, somatisation disorders.

122
Q

What is a psychotic episode?

A

At least 1 week of either hallucinations or delusions at significant severity.

123
Q

What is a delusion?

A

Firmly held belief on inadequate grounds, not affected by rational argument or evidence to the contrary, not shared by similar age, education/ cultural/ religious/ social background.

124
Q

What are the different types of delusions?

A

Include primary (delusional perception), secondary (delusion stemming from a primary delusion), persecutory (paranoia), -of reference (coincidences have meaning), grandiose, -of guilt, nihilistic (self or others cease to exist), -of passivity (thoughts influenced by external force) etc

125
Q

What is a hallucination?

A

A perception experienced in the absence of an external stimuli. Most common auditory by any sensory possible.

126
Q

Name 5 types of hallucinations.

A

Auditory hallucinations, Somatic Hallucinations, Thought insertion/withdrawal/broadcast, passivity phenomenon (external force influences you), delusional perception

127
Q

Name 6 signs of schizophrenia

A

Self neglect, Talking to themselves, posturing, clothing, perplexity, social disturbance (including unprovoked violent acts)

128
Q

What are side effects of schizophrenia medication?

A

severe weight gain, parkinsonian symptoms, tardive dyskinesias, skin discouloration. NONE ARE SPECIFIC TO SCHIZOPHRENIA– NEED INTERVIEW

129
Q

How common is schizophrenia?

A

0.2-0.7%, 2/10k per year, increasing in S London. Up to 5x incidence variation worldwide, increased in migrants

130
Q

What is the age for schizophrenic onset of each sex?

A

25-32 females, 21-26 in male (men have earlier and more negative episodes)

131
Q

What is said of the social class of schizophrenics?

A

No common social class, but lower social drift.

132
Q

What is the most likely social determinant of transition to psychosis?

A

Cannabis. Impact more potent on developing brains, schiz. pts more sensitive to cannabis than controls, familial liability expressed as sensitivity to cannabis, chronic use sensitises to effect and increases vulnerability to psychosis.

133
Q

What is the genetic risk of schizophrenia?

A

1% in general population, up to 50% in monozygotic twin. Partial penetrance (genes + environment), likely polygenic

134
Q

What can cause schizophrenia at the two stages where it’s most common?

A

Birth: Obstetric complications, prenatal infection, nutritional deficiency. At adolescence adverse life events, substance use (cannabis 6x risk), pruning of gray matter

135
Q

What structural changes in the brain are seen in schizophrenia?

A

Ventricular enlargement, reduced brain volume (less gray matter), cytoarchitectural differences in cortex and hippocampus

136
Q

What area of the brain is implicated in schizophrenia and hallucinations?

A

Paracingulate sulcus

137
Q

Describe the Wisconsin Card Sorting Task

A

Decision lead to reward or negative feedback based on untold rules, which can change without warning.

138
Q

What does the Wisconsin Card Sorting task tell us about schizophrenics?

A

Overall frontal lobe dysfunction: hypofrontality during periods of high cognitive load; increase in PFC activity in healthy volunteers absent in schizophrenics

139
Q

How are brain activity, plasticity, connectivity and synchrony organised?

A

neural Oscillations, different in patients with schizophrenia

140
Q

What is the stroop test?

A

Reading the name of a color shaded in a different color, difficulty accomplishing this in schizophrenia (both time and accuracy).

141
Q

Describe the clinical picture of acute stress

A

Lasting hours to 3 days, response to exceptionally stressful events, initial daze, mixed and usually changing picture, highly individual

142
Q

Describe the clinical picture of adjustment disorder

A

wide range of emotional of behavioural symptoms to a stressor not necessarily life-threatening, seen as out of proportion, last up to 6 months

143
Q

What prompts PTSD?

A

Witness/experience event that involves actual or threatened death or serious injury or threat to physical integrity of self or others.

144
Q

Name 6 symptoms of PTSD.

A

Re-experiencing flashbacks/nightmares, numbness, Avoidance, Hypervigilance/startle, insomnia, anxiety/depression

145
Q

What is the onset and recovery rate of PTSD?

A

Immediate onset, most recover within a year. Rape 94% at 2 weeks, 65% at 1 month, 42% at 6 months

146
Q

Who tends to have General Anxiety Disorder?

A

8.9% of population, Women > Men, 3X in primary care clinics, ~70% with co-morbidities

147
Q

What role does genetics play in general anxiety disorder?

A

Modest Role: 5X increase in 1st degree relative (19.5% vs 3.5% in controls), share heritibility for GAD and mood disorders.

148
Q

What parenting styles leads to higher rates of general anxiety disorder?

A

More protective, less caring.

149
Q

Describe the clinical picture of agoraphobia?

A

Away from home in situation cannot easily leave, presents with anxiety symptoms, anxious cognitions about faiting and loss of control are common, avoidance is common

150
Q

What environmental factors impact likelihood of panic disorder?

A

6–96% have precipitating events (separation/loss, relationship difficulties, new responsibilities), Traumatic early life events (early parent separation, traumatic childhood events 3X, early sexual abuse <5 years)

151
Q

What are the subtypes of specific phobias?

A

Blood, injection, injury; animals & insects; natural environment; situational; other

152
Q

What is the reaction of someone with a blood-injury phobia?

A

Blood-injury phobias start with a sympathetic followed by a parasympthetic response, and syncope (scream then faint), feel disgust + repulsion rather than apprehension.

153
Q

What is the reaction of someone exposed to their phobia?

A

intense anxiety that may meet criteria for a panic attack, extreme apprehension and desire to escape

154
Q

What role do genetics play in specific phobias?

A

31% of 1st degree relatives affected. Animal phobis 26% monozygotic, 11% dizygotic

155
Q

Name the 4 psyhological theories regarding specific phobias.

A

Psychoanalytic: symptoms related to unresolved unconscious conflicts; classical conditioning: negative experience + object/situation; marks’ preparedness theory: historically threatening species survival is commonly feared; phobias acquired via observational learning

156
Q

Describe the clinical picture of social phobia

A

Inappropriate anxiety during observation or potential for criticism, leads to avoiding triggers (eating in public, dinner parties, committees/seminars/public speaking)

157
Q

What are the symptoms of social phobias?

A

Anticipatory anxiety, feeling anxious, blushing, trembling, relieved by alcohol

158
Q

Describe the aetiology of social phobias.

A

Both genetic and environmental factors, genetic one third of variances, monozygotic > dizygotic twins

159
Q

Describe the clinical picture of OCD

A

Obsessional thoughts/images (resisted, intrude forcibly on mind, recognised as own), compulsions reduce anxiety, cleaning/checkin. precision “just right”

160
Q

Discuss the epidemiology of OCD

A

More women than men, more boys in adolescence, mean onset ~20yo, 2-3% prevalence

161
Q

What co-morbidities exist for OCD?

A

~67% major depressive episode, risks for anxiety disorders, higher prevalence of tourette’s syndrome

162
Q

What 2 areas make up descriptive psychopathology?

A

Observation of behaviour and phenomenology

163
Q

What are the components of a mental status examination?

A

Appearance and behaviour, Speech, Mood, Expression, Thought, Perception, Cognition (orientation, memory, and intelligence), Insight

164
Q

What are the 4 types of affective episodes?

A

Major depressive, manic, hypomanic, and mixed affective

165
Q

What is atypical depression?

A

Mood Reactivity AND significant weight gain, hypersomnia, leaden paralysis, interpersonal rejection sensitivity

166
Q

What is the HPA axis and what does it do?

A

Hypothalamus (corticotropin releasing hormone), Pituitary (adrenocorticotropic hormone), Adrenal cortex (cortisol)– acute stres response.

167
Q

What regulates the amygdala and hpa?

A

hippocampus feedback to limit cortisol production

168
Q

What happens in situations of chronic stress?

A

Increased Ca2+ entry into neurons, too much Ca2+ excitotoxic- cells die

169
Q

What type of brain damage is caused by stress?

A

Pyramidal cells dies off– shrunken hippocampus

Module 202 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions