Neuro Flashcards

1
Q

What is classical conditioning and operant conditioning

A

1) conditioned response is paired with specific stimuli
2) positive or negative reinforcement (praising good behaviour, removing something unpleasant)

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2
Q

Difference between fear and anxiety

A

1) abnormal worry to a perceived threat. Anticipation of something in the future. Urge to avoid, sense of dread
2) sense of danger. Urge to escape. Refers to here and now

-Body sensation: high HR, hot, trembling, fast breath, tense, nausea, dry mouth
-Thoughts: want to escape, something bad will happen, why am I like this
-Feelings: scared, overwhelmed, nervous

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3
Q

Symptoms of Alzeimer’s and when is best to treat them

A

-Cerebral atrophy: Reduced, Social function, intellect, speech, memory and concentration

-Dental treatment often best first thing in morning

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4
Q

What is Korsakoff’s psychosis. What deficiency is it

A

Memory deficits, confusion, and behavioral changes
-associated with chronic alcoholism
-B1/thiamine deficiency

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5
Q

Medical and dental complications of bulimia nervosa

A

[binge-eating then self-induced vomiting or exercise. Fear of becoming fat]
-Russel’s sign - calluses on the back of their fingers and traumatic lesions on their palate as a result of self induced vomiting
-Dehydration/weight fluctuations
-Low potassium and muscle cramps
-Acidosis/alkalosis
-Oesophagitis
-Poor muscular tone in the colon from laxative abuse
-Dental erosion
-Parotid enlargement
-Caution during GA due to low BMI

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6
Q

Positive and negative symptoms of schizophrenia

A

-Psychosis=Delusion, hallucination, disorganised thoughts, lack of insight

Positive
-Hallucinations: imagined inner voices. See things others don’t
-Extreme disordered thinking
-False beliefs
-Delusions, bizarre thoughts
-Unable to concentrate

Negative
-social withdrawal
-lack of drive
-low mood
-apathy
-lack of cognitive function

Cognitive deficits = disturbances of memory, attention, executive function

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7
Q

Specific dental aspects of schizophrenia

A

-Delusional beliefs (aliens controlling me through silver fillings)
-Hallucinations may be somatic/pain
-Poor general health and hygiene
-Drug, alcohol and smoking
-Medication effects – haloperidol and clozapine cause hyposalivation
-Struggle following OHI

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8
Q

Drug mechanisms for antipsychotics (1st and 2nd generation)

A

-Psychosis= increased dopamine in the mesocortical/ mesolimbic pathway (involved in mood, reward, addiction).
-1st=D2 receptor antagonists will inhibit the other pathways causing side effects of increased prolactin and tremors. Also affinity for H1, M1, a1 (sedation, dry mouth, postural hypotension etc.)
-2nd= fewer side effects as dissociate faster from the D2 receptor, and they are better at treating negative symptoms (blunted emotions, loss of energy, social withdrawal). And no affinity for H1, M1, a1

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9
Q

What are affective disorders. Give examples

A

-marked disruptions in emotions (severe lows or highs)
-depression, dysthymia, bipolar disorder, generalised anxiety, Seasonal Affective Disorder

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10
Q

Difference in symptoms for panic attack and myocardial infarction

A

-Panic= chest pain in sharp, stabbing, localised in middle chest. Occurs due to extreme stress. Usually lasts shorter. Symptoms get better over time
-MI= squeezing or pressure pain, can radiate to arm, occurs due to physical exertionor at rest, lasts longer with worsening symptoms

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11
Q

What is OCD and its symptoms

A

-repeated unwanted thoughts of sensations/ urge to do something over again
eg. Checking switches, fear of contamination, lining things up, intrusive thoughts
-Obsessions (intrusive thoughts, impulses)
-Compulsions (rituals) Eg. repetitive brushing causing bleeding/lesions/wear. Nail biting causing TMD

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12
Q

Explain generalised anxiety disorder, depression and bipolar disorder

A

1) >6 months of anxiety not confined to a specific situation affecting daily life
2) Persistent low mood and loss of interest for >2 weeks. eg. reduced motivation for OH
3) alternating high moods (mania) and low moods (depression)

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13
Q

What is hypochondriasis

A

-excessive worry about having or developing a serious undiagnosed medical condition
eg. transient dry mouth is proof of oral cancer

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14
Q

Somatization disorder

A

significant focus on physical symptoms, such as pain, weakness or shortness of breath, to a level that results in major distress and/or problems functioning
-concerned they have serious disease (eg. headache as sign of brain cancer)

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15
Q

What is psychogenic pain. List some syndrome in dentistry

A

pain with no pathology
evidence of psychological cause (anxiety, depression).
-Atypical facial pain (may be misdiagnosed as trigeminal neuralgia)
-Atypical odontalgia (continuous toothache with no cause)
-Oral dysethesia (recurring burning of oral mucosa)

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16
Q

TMJ dysfunction syndrome

A

-disturbance of balance of musculoskeletal system where there Is abnormalities in relationship between teeth and muscles
-lack of coordination
-due to muscle hypoxia and/or articular degeneration
-aggrevated by stress, psychological factors, environmental, genetic

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17
Q

Differences and similarities between TMD dysfunction syndrome and trigeminal neuralgia

A

-Similarities=pain due to activity of facial or masticatory muscles, reduction of patient’s quality of life, radiating pain
-TN= mainly unilateral, acute, stabbing, remission at night, short lasting with long periods of remission
-TMD= bilateral, dull continuous, may still present at night, long-lasting with short intermissions, worse in the morning

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18
Q

Signs and symptoms of syncope (faint)

A

-due to fear, being too hot, lack of food
-Before loss of consiousness: vessel dilation, drop in BP, dizziness, pale tachycardia >100bpm, unresponsive, light head, sweaty
-After faint: reflex bradycardia <60bpm

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19
Q

What are the 2 origins of a faint. Management of syncope

A

1) Vaso-vagal origin: autoregulation of BP, a drop in cerebral perfusion causing transient loss of consciousness
2) Carotid sinus- due to pressure put on carotid sinus (turning head, tight collar)

Get them to lie down and raise legs. Glucose drink

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20
Q

Generalised epilepsy affect both sides of brain. Difference between 1) Grand Mal and 2) Peitit Mal epilepsy

A

=Sudden uncontrolled burst of electrical activity in brain
1) Motor seizures. Tonic clonic seizure. Aura, then loss of consiousness then convulsion (jerky) Incontinence, hypersalivation
2) Absence (non-motor) seizure. Lose awareness of surroundings for a few seconds. Rapid blinking or staring into space. Mainly affects children

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21
Q

What is focal type epilepsy. The different types

A

Seizure in 1 location of your brain- partial seizures. 4 types:
1. Focal aware – aware of what’s happening
2. Focal impaired awareness – confused, remember some of it
3. Focal motor – twitch, spasm, unconscious movements
4. Focal non-motor – raised HR, goosebumps, heightened emotions

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22
Q

How to manage someone having a seizure

A

-start timer. During the first 5 mins make sure pt comfortable, remove any danger, reassure patient, do not restrain them

-If >5 mins= status epileptics. Emergency. 10mg buccal midazolam. Repeat if no response after 10 mins.

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23
Q

Mechanism of action for anticonvulsant medications. Give examples of names of drugs

A

-they inhibit rapid repetitive neurones firing to treat convulsions in epilepsy, can also treat neuralgia and neuropathic pain
-Inhibit ionic channels (Na, Ca)
-enhance GABA (increasing Cl)
-inhibiting glutamate

-Phenytoin, carbamazepine, gabapentin, Benozdiazepine

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24
Q

Oral side effects of 1) phenytoin and 2) carbamezapine

A

(anticonvulsants)
1) Gingival overgrowth, Root shortening &/or resorption, Hypercementosis, Salivary gland hypertrophy
2) Xerostomia, Glossitis, Oral ulceration, stephen johnson syndrome, liver disorders (so FBC checked every 6 weeks)

Both: Cervical lymphadenopathy, Cleft–lip and palate – avoid in pregnant women unless absolutely necessary

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25
Q

History taking for someone with epilepsy

A

-Ask what medication they are on, if their medication works
-what triggers a fit (bright lights, hunger, stress, little sleep, alcohol, excitement)
-timing of their last 3 seizures
-If meds recently changed- their previous meds likely didn’t control their symptoms so may want to defer treatment until been on their new meds for a couple months

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26
Q

Febrile convulsions

A

-epileptic type symptoms, but not epilepsy
-Common in infancy but grow out of them. Brought on by very high temperature secondary to infections
-Treated by bringing down temperature- paracetamol, fans

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27
Q

What is multiple sclerosis. Symptoms.

A

-autoimmune condition where body attacks brain and spinal cord causing demyelination of nerves
-fatigue, vision problems, numbness, tingling, muscle spasms/stiffness/weakness/atrophy, mobility problems, pain, problems with thinking/learning/planning. Difficulty controlling bladder, coordination/balance issues

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28
Q

What is Parkinson’s. What part of the brain is affected and what abnormal proteins accumulate there. Symptoms

A

-degeneration and loss of nerve cells in substantia nigra due to Lewy bodies and neurtites, due to ageing, head injury or cerebrovascular disease
-reduced dopamine, which results in increased Ach
-Nigrostriatal pathway affected
-Involuntary shaking (pill-rolling tremor common), rigidity on movement, bradykinesia (slow), restless, expressionless face, stooped posture, fatigue cognitive decline, postural hypotension, hypersalivation

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29
Q

What is parkonsonism

A

-umbarella term for a group of disorders with symptoms of slow movement, tremor at rest, involuntary movement, stiff, fatigue, drooling, postural instability
-causes: Parkinson’s disease (neurological disorder), toxins, drugs, brain injury, infection

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30
Q

Effects of dopamine. What are the 3 pathways

A

-Tyrosine enters presynapse and converted to DOPA then DA and then released.
1- Nigrostriatal pathway: controls fine movements. Reduced DA (in Parkinson’s) causes tremors, muscle rigidity and loss of facial expression
2-Mesocortical/ mesolimbic pathway: controls mood and reward so increased DA here causes psychosis
3-Tuberonifundibular: DA also acts as a hormone when released form hypothalamus and acts on ant pituitary. Inhibits prolactin

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31
Q

Dopaminergic medications used in Parkinson’s disease - Different types and their actions. Side effects

A

Increase dopamine

  1. Precursor of DA
    eg. Levodopa
  2. COMT inhibitors- decrease DA metabolism (entacapone, opicapone)
  3. Dopamine agonists
  4. Dopamine release stimulators

Dry mouth (=taste disturbance, stomatitis, ulcers) headache, dyskineasias (involuntary movements)

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32
Q

What is the issue with Levodopa for treating Parkisnon’s

A

-becomes less effective over time
-Motor fluctuations and dyskinesia develop in the majority of people who take levodopa long term. So only used short term
-causes BMS

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33
Q

Side effects of Muscarinics used to treat Parkinson’s.

A

decrease Ach (as it increases as a result of decreased dopamine)
Although not used routinely - cause dry mouth as decrease parasympathetic activity

34
Q

What are “on and off” times in Parkinson’s

A

-‘On’ time is when levodopa is working well and symptoms are controlled. Usually within 60-90 mins of meds
-Off’ =no longer working well causing tremor, rigidity and slow movement to re-emerge.

Make sure dental appointments are short and better to have in morning, after Levodopa dose

35
Q

Will head ache from a brain tumour be worse in the morning or evening

A

Pressure gradually decreases throughout the day - Headaches characteristically worse in morning

36
Q

What is myasthenia Gravis

A

-Muscle weakness and atrophy
-long-term antibody-mediated autoimmune disease
-Deficiency of functioning Ach receptors
-droopy eye lid, double vision, difficulty making facial expression, swallowing and chewing issues

37
Q

What is Bulbar palsy. What nerves are affected

A

-impacted lower cranial nerves connecting brain stem to muscles
- CN9,10,11,12.
-Disrupts motor control: palsy of tongue, swallowing, speech, reduced gag reflex.
-caused by brainstem strokes, brainstem tumours, infection, autoimmune diseases (Guillain Barre)
-A LMN lesion

38
Q

What is Ramsay Hunt syndrome and cause

A

-Reactivation of Varicella Zoster virus in geniculate ganglion of facial nerve causing ipsilateral facial paralysis
-vesicles in pharynx and near the ear

39
Q

Meningitis. Symptoms and Management

A

-Inflammation in meninges that protects the brain and spinal cord
-Viral and Bacterial (more common and serious)
-severe headache, fever, nausea, stiff neck, photophobia, seizures
-purpuric rash that does not fade when role glass over it
-can cause blood poisoning, sepsis, permanent changes to brain and nerves if not treated, vision loss, hearing loss
-IV antibiotics, fluid, oxygen

40
Q

What is spina bifida. causes, symptoms

A

-Neural tube defect: Vertebral arches fail to fuse (potentially due to folic acid deficiency during pregnancy)
-babies spine doesn’t develop properly. Gap in spine, inability to walk, epilepsy, learning difficulties, leg weakness

41
Q

the 2 types of stroke. which is more common

A
  1. Ischaemic -90% of stokes= Cerebral infarction, arterial occlusion from atherosclerosis, thrombosis, embolism
  2. Haemorrhagic – 10% = bleeding from intracerebral vessel

disturbance of blood supply to brain. Lose neurological function

42
Q

Stroke risk factors

A

-Age
-Hypertension (most important)
-Smoking
-Hyperlipidaemia (more important for MI)
-Diabetes
-Coagulation disorders.
-Atrial fibrillation (intracardiac thrombus causing cerebral embolism) = atria doesn’t contract, get blood clots in atria which can embolise into the circulation which can cause strokes

43
Q

Primary and secondary prevention for strokes

A

-Primary (before the stroke. eg. If have AF) Secondary (after had a stroke)

-Lose weight, decrease salt, reduce alcohol
-Antihypertensives (ACEI)
-Anti-platelets (aspirin, clopidogrel, dipyridamole)
-Anticoagulants (DOACs)
-Statins- lipid lowering

44
Q

What artery is occluded in total anterior circulation stroke (TACS) How this differs to (PACS)

A

-Occlusion of MIDDLE CEREBRAL ARTERY
-affects motor & sensory, visual, speech & neglect

-PACS= partial anterior circulation stroke
-less severe

45
Q

Lacunar stroke (LACS) and posterior circulation stroke (POCS)

A

LACS= small stroke, only affecting one of motor/sensory, visual, speed/neglect

POCS= affects cerebellum affecting balance and cranial nerves

46
Q

Management of acute stroke

A

-Full neuro assessment, ECG, CXR, U&E, glucose, lipids, FBC
-CT scan- to decide if haemoragic. If haemorhagic =stop anticoagulants, control BP
-If ischaemic: IV thrombolysis within 4.5 hours to dissolve clot
-Aspirin and clopidogrel. Then stop aspirin after 2 weeks
-Continue monitoring.
-Preventative meds: Statin, DOAC

47
Q

Explain dysarthria, dysphonia and dysphasia

A

-Dysarthria = DIFFICULTY IN ARTICULATING SPEECH - slurred
-Dysphonia = LOSS OF VOICE – hoarse/ lack of voice
-Dysphasia = LOSS OF CEREBRAL LANGUAGE SKILLS – can’t find/ think of words

48
Q

Symptoms when Stroke in 1) Wernicke’s area and 2) Broca’s area. What lobes are they in

A

1) cannot comprehend. Temporal
2) cannot form words or sentences (BROCken speech) Frontal

49
Q

Symptoms of dysphagia

A

Difficulty swallowing. Oral, pharyngeal and oesophageal stage can be affected
- formation of bolus, elevation of pharynx, closure of soft palate and glottis, propulsion into oesophagus peristaltic propulsion towards cardiac sphincter, and into stomach.

50
Q

List causes of dysphagia

A

-xerostomia
-stokes
-Barett’s oesophagus
-MND
-multiple sclerosis
-cancer
-GORD
-bulbar palsy
-myasthenia gravis

51
Q

Ways of assessing swallowing problems

A

-barium swallow
-gastrointestinal endoscopy
-SALT assessment
-endoscopy and CT if suspected cancer

52
Q

What is achalasia

A

problem with plexus of nerves that controls peristalsis = oesophagus doesn’t squeeze properly -oesophagus full of food rather than stomach full of food

53
Q

What are the sensory and motor neves

A

Some say marry money but my brother says big, brains, matter, more

54
Q

Which nerves are parasympathetic

A

3,7,9,10

CNIII- pupil contraction
CNVII- submandibular, sublingual gland
CNIX-parotid
CNX- lowers HR etc.

55
Q

CNI test

A

Olfactory nerve
-ask if change to sense of smell
-use standard smell bottles using 1 nostril

56
Q

CNII test

A

Optic nerve
-Visual acuity=Schnellen test 1 eye at a time (keep glasses on)
-Accomodation=follow finger to eye
-Visual neglect= tell me which finger is moving
-Visual field=cover 1 eye and bring finger into periphery
-Pupillary =torch

57
Q

CNIII, IV and VI nerve test

A

Occulomotor (3) Trochlear (4) Abducent (6)
-Eye movement- Get them to follow pen or finger in a letter H.
-Ask if any diplopia
-Pupil constriction with torch (CN3)
-Eye lid for ptosis (CN3)

58
Q

Which eye muscle do the CN3,4 and 6 innervate. What if they are damaged

A

3) Occulomotor - all other extra ocular muscles (damaged= ptosis, impaired movement, eye looks down and out, pupil dilation)
4) Trochlear- superior oblique (damage= diplopia, eye look up and in)
6) Abducens- lateral rectus (damage=can’t look laterally, cannot align eyes so diplopia)

59
Q

CNV nerve test

A

Ophthalmic, maxillary and mandibular divisions of the trigemnal nerve (V1, V2, V3)
-Sensation of face-gently brush both sides of forehead, cheeks and jaw and ask if they can feel it and if it feels equal on both sides
-strength of MOM: clench their jaw and palpate masseter. Push on lower border of chin and ask them to open their mouth
-Reflexes- jaw jerk, corneal reflex

60
Q

CNVII nerve test (and explain which branches you are testing)

A

Facial nerve
-Muscles of facial expression
Temporal: raise eyebrows
Zygomatic: scrunch eyes
Buccal: blow out cheeks
Mandibular: big smile
Cervical: tense neck muscles

Sense of taste anterior 2/3 (chords tympani)- ask about change in taste

61
Q

CNVIII nerve test

A

-Vestibular- get then to stand up and close eyes
-Cochlear - Weber’s, Rinne’s test to test if conductive or sensory hearing loss

-Rinnes- Tuning fork on mastoid then in front of ear. If BC>AC then conductive hearing loss
-Weber’s-Fork in middle of head, ask which side is louder. If sound is heard better in right ear then left ear has sensory hearing loss.

62
Q

CNIX and X nerve test

A

Glossopharyngeal and vagus
-check soft palate: get them to say aah and look for symmetry of soft palate going up
-check can cough
-Check swallow
-Check voice

63
Q

CNXI nerve test

A

Accessory nerve (trapezius and SCM)
-Shrug shoulders, then apply pressure for resistance
-Turn head left and right against resistance

64
Q

CNXII nerve test

A

Hypoglossal
-tongue range of movement-
say days of week quickly, say baby hippopotamus
-poke tongue at side of cheek
-stick out tongue

65
Q

What if tongue deviated to right

A

nerve weakness on right of hypoglossal

[overpowering on left]

66
Q

Uvula deviated to right. Is there palsy in left or right side

A

Glossopharyngeal nerve is weak on left
[think of pully system]

67
Q

Causes of cranial nerve damage

A

-trauma
-tumour, stoke (UMN)
-brainstem lesion
-8: Paget’s disease, acoustic neuroma
-increased intraocular pressure
-Multiple sclerosis
-cavernous sinus infection (3,4,5,6)
-bulbar palsy (9,10,11,12)
-Bell’s palsy, Ramsay hunt= 7
-polio-11

etc.

68
Q

Difference between upper and lower motor neurone for facial nerve. Causes

A

-LMN= Total weakness on affected side. eg. Bell’s palsy, Ramsay Hunt, vestibular schwanoma (virus, autoimmune)
-UMN= Palsy on opposite side. Forehead spared. Due to stroke, tumour, MS

69
Q

Difference between NREM and REM sleep. Which is increased and which is deceased with drug-induced sleep

A

-75% Non-Rapid Eye Movement (NREM) [N1-4]
-25% Rapid Eye Movement (REM) - dreaming, relaxed

Drug-induced=Increased NREM, decreased REM, so improve length but still not as good as physiological sleep

70
Q

Diazepam and midazolam: which is longer lasting, has longer half life, uses, more potent, lipophilic, painful on injection. Administration, uses and metabolism

A

-Diazepam= longer lasting, insoluble in water, long half life, pain on injection
-Midazolam= short acting, water soluble, lipophilic, painless, short half life, more potent

Both: IV, liver metabolism, seizures, fits, anxiety, sedation

71
Q

Benzodiazepine action and side effects

A

-Action= enhance GABA which is inhibitory, increases opening frequency of Cl channels, decreasing excitability. 3 sites of action:
1. RAS=hypnotic effect
2.Limbic= anxiolytic
3. Cortex=anticonvulsant

-rebound effects, dependance, addiction, respiratory depression, reduced BP, compensatory high HR
-synergistic CNS depression with opiates, alcohol, antihistamines

(barbiturates increase duration of channel opening so more toxic)

72
Q

What is the benzodiazepine reversal drug

A

-Flumazenil - antagonist, stronger binding than other benzodiazepines

73
Q

Action of anti-histamines

A

Suppress immune system by blocking H1 receptors
Causes vasodilation, bronchodilation

74
Q

List drug types that are 1) hypnotics, 2) anxiolytics

A

1) BDZ, anti-histamines, barbiturates, alcohol, zopiclone
2) BDZ, B blockers (propranolol), alcohol, Serotonergic (Buspirone)

75
Q

Action of Busiprone

A

-Acts as a serotonin receptor agonist
-Does not cause sedation – ANXIOLYTIC WITHOUT SEDATION
-takes 2 weeks to have effect
-causes dry mouth

76
Q

What 2 BDZs can dentists prescribe

A

Temazepam and diazepam (plus flumazenil)

77
Q

What are catecholamine hormones and receptors

A

hormones made by adrenal glands. Dopamine, noradrenaline and adrenaline
- The receptors are called adrenoreceptors. For example a1, B1 (in heart) and B2 (in lungs)

78
Q

What hormones are low in depression. Action of antidepressants (TCAs, SSRIs, SNRIs, monoamine oxidase inhibitors)

A

-reduced levels of 5HT and NA
1. TCAs: inhibit reuptake of 5HT and NA by blocking transporters so it increases neurotransmission.
- However, have affinity for H1, M1 and a1 receptors so cause side effects such as sedation, dry mouth, postural hypotension. And effects are delayed so feel worse before better.
2. SSRIs (1st line) selective so don’t bind to other receptors. Block 5HT reuptake, increasing neurotransmission.
3. SNRIs: selective, block 5HT and NA reuptake
4. Monoamine oxidase inhibitors: block metabolism of 5HT and NA so more is recycled so neurotransmission increases

79
Q

What is Horner’s syndrome- causes and symptoms

A

unilateral contracted pupil, drooping upper eyelid (ptosis), sunken eye, and local inability to sweat on one side of the face (anhydrosis)

-caused by damage to sympathetic nerves on that side of the neck - neck trauma, infection, cancer

80
Q

Causes of an 1) extradural and 2) subdural haematoma. Which occurs more slowly

A

1) middle meningeal artery damage. Very quick onset. Due to skull fracture. Convex on MRI
2) Occurs more slowly. Symptoms present few days after. Venous bleeds, Crescent shape. May be mistaken for dimentia

81
Q

CAGE method of assessing potential alcohol abuse

A

C - Have you ever felt you should CUT down?
A - Are you ANNOYED if people comment on your drinking?
G - Do you feel GUILTY about the amount you drink?
E - Have you ever drank EARLY in the morning as an eye-opener?

If 2/4 of these are answered yes, a problem is indicated.