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Human Diseases Yr4 > Neurological disorders > Flashcards

Neurological disorders Flashcards

1
Q

What are the origins of syncope (fainting)? Why does it occur?

A

Vaso-vagal origin usually, can be carotid sinus
Occurs due to overactivity of sympathetic nervous system (initially tachycardic, when fainting theres a reflex bradycardia)

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2
Q

What questions should you ask someone who presents with epilepsy in their MH?

A
  • Precipitating factors/ any warning?
  • Does the medication work in controlling seizures?
  • When was the last seizure?
  • Any change in medication
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3
Q

What is a Grand Mal seizure/ Generalised motor seizure?

A

Classically preceded by an aura, LOC follows leading to convulsions. Tonic phase where muscles contracted giving way to clonic phase where theres repetitive jerky movements, increased salivation and marked bruxism. Altered breathing, cyanosis and tongue biting. Affects both sides of brain.

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4
Q

What is Status Epilepticus?

A

Grand Mal seizure that has continued for 5+ mins/ doesnt have a proper end. Medical emergency as pt can become hypoxic

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5
Q

What is Absence Seizure/ Petit Mal/ Generalised non-motor seizure?

A

Seen in children- speech/attention affected (not to be confused with febrile convulsion in pyrexic child). Pt stops what they are doing and stares, may do repetitive movements. Affects both sides of brain.

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6
Q

What is a Stokes-Adams Attack?

A

Result of cardiac arrythmias, often no warning or palpitations, drop attacks - LOC

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7
Q

What is a partial seizure/focal epilepsy?

A

Can be simple = clonic movements of a group of muscles/limbs or complex = involving hallucinations. Develops in one side of brain. 4 types: 1) Focal aware 2) Focal impaired (confusion) 3) Focal motor (spasm) 4) Focal non-motor (changes in thought)

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8
Q

What is a TIA? What medication is a patient put on?

A
  • Sudden onset of focal CNS signs due to temporary occlusion of part of cerebral circulation (usually secondary to atheromatous deposits in carotid artery)
  • Resolves less 24 hrs
  • Indicators of stroke risk
  • Usually put of 75mg aspirin
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9
Q

What is multiple sclerosis?

A

Demyelination of the myelin sheath resulting in short circuits. Can have sensory and motor symptoms e.g. optic neuritis causing visual disturbances, weakness or paralysis of limbs, nystamus (involuntary rapid movement eyeballs), ataxia (uncoordinated involuntary movement), loss of sphincter control causing difficulting swallowing or incontinence. Viral aetiology postulated.

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10
Q

What treatment is given for multiple sclerosis which can help long term prognosis?

A

Steroids

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11
Q

What is Parkinsons Disease?

A

Degeneration of the pigmented cells of the substania nigra leading to dopamine deficiency. May result form previous head injury or cerebrovascualr disease. Presence of Lewy bodies (abnormal protein aggregates in nerve cells) and neurites. Affects 1% >60year olds

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12
Q

What are the signs and symptoms of Parkinsons disease?

A
  • Pill rolling tremor
  • Cog wheel rigidity on movement ie stop/start
  • Bradykinesia ie slow movement
  • Akathisia ie restless movement
  • Expressionless face
  • Stooped posture
  • Shuffling gait
  • Impaired autonomic function leading to postural drop in BP
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13
Q

What difficulties can occur for a patient with motor neurone disease?

A
  • Dysphagia - difficulty swallowing so can develop aspiration pneumonias
  • Respiratory difficulties - given tracheostomy
  • Suffer from ascending infection e.g. UTI
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14
Q

What is myasthenia gravis?

A

Antibody mediated autoimmune disease with a deficiency of functioning Ach receptors. Commonly affects young women and presents with muscles getting tired when they are working

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15
Q

Are brain tumours more common as primary or metastases?

A

Metastases - from lung, breast, GIT and kidney

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16
Q

What is Eaton-Lambert syndrome?

A

Seen in patients with lung/other cancers where muscles get stronger rather than weaker with activity

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17
Q

What is bulbar palsy? What cranial nerves does it affect?

A
  • Palsy of tongue, MoM, swallowing and facial muscles due to loss of function of motor nuclei in brainstem
  • Caused by infection e.g. polio, guillain Barre (acute) or tumour (chronic)
  • Affects IX, X, XI, XII
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18
Q

What long term drug use can cause tics/ involuntary facial movements?

A

Phenothiazine

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19
Q

What is Ramsay-Hunt Syndrome (EXAM Q)?

A

Profound facial paralysis with vesicles in the pharynx and external auditory meatus of the same side. Geniculate ganglion of VII is infected with herpes zoster.

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20
Q

How can bacterial meningitis occur in maxillofacial injuries? What is worse, bacterial or viral?

A

Injuries involving the mid third of face (cribiform plate and cranial base) can get ascending infection into the meningeal layers of the brain (Dura =outer, arachnoid, pai mater =inner)
Viral milder and self-limiting

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21
Q

What are the signs of meningitis?

A
  • Kernig’s sign - legs flexed 90 degrees at hips and resistence to extending knee
  • Severe headache
  • Nausea/vomiting
  • Painful still neck
  • Photophobia
  • Purpuric rash (doesn’t fade on pressure)
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22
Q

How can brain abscesses occur?

A
  • Secondary to infection e.g. oral sepsis, infection of middle ear, paranasal sinus infection
  • From septic emboli in patients with congenital heart disease
  • Complication of infective endocarditis
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23
Q

What are the 3 main types of cerebral palsy?

A

1) Spastic = muscles contracted
2) Ataxic = disturbance of balance
3) Athetoid = writhing movements

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24
Q

What is cerebral palsy?

A

Disorder of motor function secondary to cerebral damage - frequently associated with birth injury or hypoxia

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25
Q

What is spina bifida?

A

Vertebral arches fail to fuse - thought to be due to folic acid deficiency. Causes inability to walk, epilepsy or learning difficulties. May be associated with hydrocephalus (retention of CSF in brain)

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26
Q

What are 2 distinct clinical features of spina bifida?

A
  • Tuft of hair at base of spine
  • Meningocele - where meningeal layer surrounding spinal cord herniates out between the bones of vertebrae (usually lumbar)
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27
Q

What is Huntington’s Chorea?

A

Progressive dementia with marked involuntary movements. Autosomal dominant and early onset of middle age.

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28
Q

What is a stroke?

A

Sudden focal loss of neurological function due to disruption of blood supply to part of the brain - permanent damage and disabling

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29
Q

What are the 2 main pathophysiologies/causes of a stroke?

A

Ischaemic, infarction, occlusive stroke (90%)

  • Atherosclerosis (artery fatty deposit)
  • Thrombosis (blood clot forms on plaque)
  • Embolism (solid material from somewhere else e.g. travelling blood clot)

Haemorrhage (10%)

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30
Q

How can you tell if there has been a cerebral haemorrhage from a CT scan?

A

White - RBC have iron which absorb x rays

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31
Q

How can you tell if there has been an ischaemic stroke from a CT scan a)mild b) severe?

A

a) Subtle changes e.g. sulci on brain less visible

b) Dark from infarction

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32
Q

What are the risk factors of a stroke?

A
  • Age
  • Smoking
  • Diabetes
  • Hypertension
  • Coagulation disorders
  • Atrial fibrillation
  • Hyperlipidaemia
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33
Q

What measures can be taken to prevent strokes?

A
  • Treat risk factors (Primary prevention)
  • Medications (Secondary prevention): antiplatelet (aspirin or clopidogrel), anticoagulants (warfarin or newer NOACs e.g. dabigatran, apixaban)
  • Surgery if carotid arteries narrow: surgical endarterectomy for stroke due to carotid stenosis
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34
Q

Clinical stroke syndromes depend on site and severity of damage. What do the following stand for?

a) TACS
b) PACS
c) LACS
d) POCS

A

a) Total anterior circulation stroke
b) Partial anterior circulation stroke
c) Lacuna stroke
d) Posterior circulation stroke

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35
Q

What test is used in hospitals to recognise stroke? What test do members of the public use?

A

ROSIER scale: 1 point for asymmetrical arm, leg or face weakness, speech disturbance or visual field defect. -1 point for LOC or seizure
1-6=likely stroke. -2-0= stroke unlikely

FAST

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36
Q

Once a patient is in hospital, what is the acute stroke management?

A

Thromolysis within 4.5 hrs to dissolve blood clots
CT head, ECG, CXR, FBC, lipids, clotting, U+E, glucose
Careful monitoring
Aspirin once haemorrhage excluded - clopidogrel for long term

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37
Q

What is a transient ischaemic attack (TIA)?

A

Transient focal neurological deficit lasting less than 24 hours, usually less than an hour

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38
Q

What do the following mean?

a) Dysarthria
b) Dysphonia
c) Dysphasia - expressive and receptive

A

a) speech slurred
b) can’t produce voice
c) higher cerebral function not working: expressive = Broca’s - can’t find the word. Receptive = Wernicke’s - can’t understand what is said

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39
Q

What are the 3 phases of swallowing and which phases does a stroke affect?

A

1) Oral = mastication, bolus, back of mouth
2) Pharyngeal = semi-voluntary, propelled back, epiglottis closes to protect airway
3) Oesophageal = involuntary and automatic

Affects 1 and 2 more

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40
Q

What are some causes of dysphagia?

A
  • Stroke - danger of aspiration pneumonia as no cough reflex
  • Neurological disease e.g. motor neurone
  • Oesphageal motility disorders
  • Mechanical obstruction e.g. oesophageal cancer, benign stricture from reflux scarring, extrinsic compression from lung cancer
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41
Q

What assessments would be done if you suspect problems swallowing are due to:

a) Oropharyngeal reasons
b) Oesophageal dysmobility
c) Oesophageal obstruction
d) Suspected cancer

A

a) SALT and videofluoroscopy (swallowing Xray)
b) Barium swallow
c) Barium swallow or endoscopy
d) Endoscopic biopsy, CT scan

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42
Q

What is offered in the following treatments

a) Neurological
b) Mechanical
c) Diet modification
d) Tube feeding

A

a) SALT
b) Dilation, stent, surgery
c) Puree
d) nasogastric, PEG feeding (percutaneous endoscopic gastrocopy endoscope through abdominal wall into stomach)

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43
Q

What compensatory mechanisms are part of intracranial pressure autoregulation?

A
  • Decreasing the production of CSF

- Restricting blood flow to brain by vasoconstriction

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44
Q

What are the indications of a head injury?

A
  • Scalp wound
  • Fracture
  • Dizziness, blurred vision
  • Swelling, bruising
  • Loss of consciousness
  • Stiff neck, numbness
  • Watery clear discharge out of nose/ears indicated cranial base injury
  • Headache
  • Nausea vomiting
  • Difficulty remembering incident
  • Sensitivity to light
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45
Q

What should you do if there has been a scalp injury?

A
  • Bleeds profusely so apply direct pressure
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46
Q

What are skull injuries divided into?

A
  • Open skull fractures (compound fracture)
  • Closed skull fracture
  • Basal skull fracture
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47
Q

What is a primary (direct) brain injury?

A

Occurs at time of original insult, direct damage to prain parenchyma and associated with vascular injuries

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48
Q

What is a primary (direct) brain injury?

A

Occurs at time of original insult, direct damage to brain parenchyma and associated with vascular injuries. Brain tissue can be lacerated, punctured or bruised. Damage irreversible - can debride.

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49
Q

What is a secondary brain injury?

A

Damage after initial insult. Expanding mass lesions, swelling, bleeding quickly. Increased intracranial pressure or brain herniation

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50
Q

What is a concussion?

A

Transient alteration in neurological function. Mild injury from blunt trauma with no detectable brain damage but short term memory loss

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51
Q

What is a contusion?

A

A bruised brain from closed head injuries where the brain has hit the inside of the skull. Unconsciousness can occur. Remember contrecoup effect (other side of brain)

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52
Q

What is a diffuse axonal injury?

A

Rotational forces on the brain causing snapping and stretching of axons. Disturbance can produce temporary or widespread damage, coma or death.

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53
Q

What is a sub-dural haemotoma?

A

Blood between dura mater and arachnoid - slow bleeding as venous from cortical bridging veins.
Can cross sutures, crescent shaped on CT.
Loss of consciousness and common in elderly due to cerebral atrophy and anticoagulants.

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54
Q

What is an extra-dural haematoma?

A

Blood between dura and skull base - quick as artery (middle meningeal artery). Skull fractures in temporo-parietal region
Cannot cross sutures, lens shaped on CT, lucid interval

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55
Q

What is an intracerebral haematoma?

A

Blood within the brain parenchyma

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56
Q

What are the symptoms of an early intracranial haemorrhage?

A
  • Nausea
  • Severe head pains
  • Dizziness
  • Sleepiness
  • Unequal pupil size
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57
Q

What are the symptoms of late intracranial haemorrhage?

A
  • Convulsions
  • Deteriorating consciousness
  • Increased BP
  • Slow pulse
  • Slow respiration
  • Neck rigidity
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58
Q

What imaging techniques are used in a brain injury?

A

X-rays - show bone only

CT and MRI - show more anatomy and density of blood

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59
Q

What are the layers of the brain outer to inner?

A

Skull - dura mater - arachnoid mater - subarachnoid space - pia mater - brain

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60
Q

What is the management of a patient presenting with a head injury?

A

1) ABCDE - intubate comatose pt <8GCS and immobilise spine
2) Neurological evaluation - ACVPU, GCS, treat intracranial pressure (IPC bolt to monitor <8GCS pt), manage seizures
3) Radiological evaluation
4) Treat acute injuries - direct = oxygenation and perfusion and ICP, intracranial haematomas = if subdural then craniotomy for evacuation, if intra-parnchymal then no surgery, treat ICP medically (osmotic diuretic mannitole)

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61
Q

What is GCS?

A

Eye opening response up to 4 points, verbal response up to 5 points, motor response up to 6 points.
3=comatosed, 15= fully alert

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62
Q

What is a subarachnoid haemorrhage? What causes this?

A

Bleeding beneath the arachnoid membrane

Burst cerebral aneurysms

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63
Q

What does ACVPU stand for?

A
  • Alert
  • New onset confusion
  • Responds to voice
  • Responds to pain
  • Unresponsive
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64
Q

Define these words: a) Catelepsy b) Ambivalence c) Psychosis d) Dementia e) Neurosis

A

a) Trancelike state with holding of 1 pose for a long time
b) Feeling of conflicting emotions about the same person/issue
c) Extreme disordered thinking - pt doesn’t know they have it
d) Disorder of multiple cognitive defects (mainly in elderly)
e) Pt knows they have disordered thinking

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65
Q

a) What is alzheimers disease?
b) Who does it effect?
c) What causes it?
d) What are the symptoms?
e) What are the implications for dental treatment?

A

a) A form of dementia (not all dementia pts have this)
b) 20% people over 80 years
c) Genetic and ?environmental factors. ?cerebral atrophy in old age
d) Reduced social function, intellect, speech, memory and concentration, onset insidious and pt unaware of impairment

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66
Q

What are the complications of alcoholism?

A
  • Injuries
  • Nutritional defects
  • Brain damage, epilepsy and myopathy
  • Cardiomyopathies
  • Gastritis
  • Pancreatitis
  • Liver damage
  • Social problems
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67
Q

What is Korsakoff’s Psychosis?

A

Amnesia of recent events, impaired ability to learn new tasks, fabricated descriptions of recent events (confabulation) otherwise alert and normal - due to chronic alcoholism causing thiamine deficiency (B vit)

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68
Q

What are the medical complications of bulimia?

A
  • Dehydration/weight fluctuations
  • Low potassium causing muscle cramps
  • Dental erosion
  • Acidosis/alkylosis
  • Oesophagitis
  • Poor muscular tone in colon from laxative abuse
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69
Q

What signs should you look for if you suspect self-induced vomiting?

A
  • Calluses on back of finger (Russel sign)
  • Traumatic lesions on back of palate
  • Dental erosion
70
Q

Define the following: a) Obsessive-compulsive b) Paranoia c) Sociopathy d) Dependency e) Somatoform disorder

A

a) Characteristics of inflexibility and perfection
b) Extreme unfounded mistrust of others
c) Antisocial behaviour having an unusually callous disregard for others
d) Abnormal submissiveness especially in adulthood
e) Pts preoccupied with imagined physical defects in their body - pt focuses on symptoms and investigations are negative

71
Q

What are the common symptoms of schizophrenia?

A
  • Hallucinations - perceptions in the absence of external stimulus - imagined inner voices that direct pts life
  • Psychosis - extreme disordered thinking affecting pts ability to complete activities of daily living
  • Delusions - false beliefs which are fixed and not amenable to reason - often of being persecuted
  • Passivity phenomena - pts deel they are passive bystanders in their thoughts/actions - e.g thoughts are inserted into head from others or people can hear thoughts
72
Q

What should you look out for is you suspect a pt has body dysmorphic disorder?

A
  • Seeks medical intervention e.g. veneers, ortho, teeth whitening
  • Unlikely to be pleased with result and demand further Tx
  • Depressed/suicidal
  • Will not accept psychological explanation
73
Q

What are the uses of hypnotic drugs?

What are the 4 classifications of hypnotic drugs?

A
  • Before surgery, during a life crisis (short term), supplement to pain control
  • Benzodiazepines, antihistamines, miscellaneous, barbiturates
74
Q

What does physiologic sleep comprise of?

A

75% non-rapid eye movement (NREM)

25% rapid eye movement (REM)

75
Q

What are the sleep phases in NREM?

A 
N1 = light sleep 
N2 = asleep 
N3= Best sleep - muscles relax, energy restored, BP, RR decrease 
N4 = delta wave
76
Q

What occurs in REM sleep?

A

Dreaming, body relaxed and immobile. Provides energy and supports daytime performance

77
Q

What occurs in drug induced sleep?

A

Increased NREM, decreased REM

78
Q

What are the effects of Benzodiazepines?

A
  • Hypnotic
  • Anxiolytic
  • Anticonvulsant (e.g. epileptic fit for 5 mins given medazolam)
  • Amnesic - won’t remember procedure
  • Highly addictive - side effect = dependence
  • Muscle relaxant - side effect = respiratory depression
79
Q

What BZD drugs are used as hypnotics for

a) initial insomnia
b) early morning wakening

A

a) Tamazepam, Loprazolam = shorter time, less hangover

b) Nitrazepam = longer acting

80
Q

How should pts be withdrawn from BZD?

A

Slowly to avoid rebound insomnia and anxiety, worst after acute withdrawal of short acting drugs

81
Q

What is the site of action for Benzodiazepines?

A
  • Reticular activating system = controls conscious, alert state (hypnotic effect)
  • Limbic system in cortex = controls emotion (anxiolytic effect)
82
Q

What is the MOA for Benzodiazepines?

A

Influence GABA at chloride channel to increase frequency of channel opening

83
Q

What drug is used to reverse the affects of BZD and Z drugs?

A

Flumazenil - antagonist with stronger binding but induces seizures so use carefully

84
Q

How are antihistamines used as hypnotics?

A

H1 blockers produce CNS depression at therapeutic doses. Promethazine used in children

85
Q

What are the Z drugs used for insomnia and are less likely to become dependent on than BZD?

A

Zolpidem and Zopiclone

86
Q

What are the uses of anxiolytics (sedatives)?

What are the drugs that have anxiolytic effects?

A
  • Pre-med, sedation, muscle relaxants e.g. TMD and dislocation, emergency drugs e.g. epilepsy, amnesic effect
  • Alcohol, BZD. Buspirone, Beta-adrenergic blockers
87
Q

In alcohol consumption, how long does it take to reach peak plasma levels and how long until sedation? How are patients withdrawn?

A

30 mins, 60 mins

Decreasing dose of sedative. Chlordiazepoxide used (BZD)

88
Q

Which two BZD are in the Dental formulary and what is the max no of days it can be prescribed for?

A

Diazepam (for short term muscle relaxant) and Temazepam

5 Days

89
Q

What is Buspirone? What are its effects?

A

An azapirone = specific seratonin receptor agonist that does not act on BZD receptor
Used in anxiety, does not cause sedation, no withdrawal, causes dry mouth

90
Q

What are beta-blockers used for?

A

Treating somatic anxiety e.g. tremor, palpitations = propanalol. Doesn’t stop anxiety feeling just symptoms. Not used in dental pts

91
Q

What drug is the ‘gold standard’ anxiolytic?

A

Benzodiazepines

92
Q

The international classification of disease version 10 outlines what categories for mental health disorders?

A

1) Organic (physical cause) mental disorders
2) Psychoactive substance abuse
3) Behavioural syndromes with physiological disturbance
4) Schizophrenia and delusional disorders
5) Personality disorders
6) Learning difficulties
7) Mood disorders
8) Neurotic stress related and somatoform disorders
9) Disorders of psychological development
10) Childhood behavioural disorders

93
Q

When is anxiety deemed as pathological?

A

When the feeling becomes to intense, frequent or persistent and interferes with functioning of the individual.

94
Q

What are the psychological and physical symptoms of anxiety?

A 
Psychological 
- Sense of dread 
- Irritability 
- Fear or loss of control 
- Avoidance 
- Panic 
Physical 
- Palpitations 
- Shortness of breath 
- Chest pain 
- Butterflies 
- Sweating 
- Dry mouth 
- Nausea
95
Q

What is generalised anxiety disorder?

A

Anxiety not confined to specific situation but is pervasive (everything) - experienced more days than not, ‘trait anxiety’ pt prone to worrying, anxiety rises in stressful situations

96
Q

What are panic attacks?

A

Anxiety so intense theres an overwhelming feeling of panic, identifiable trigger, short lived, feels like having heart attack

97
Q

Define phobia

A

A fear out of proportion to the stimulus which is irrational and cannot be reasoned away. Linked to a specific stimulus and present from childhood

98
Q

What cycle increases the likelihood of anxiety being experienced in similar situations and increases the chance of further avoidance?

A

‘Avoidance/relief’

99
Q

How can you manage dental anxiety through a) preventing it b) treating it?

A

a) Calm sympathetic approach, honest tactful explanations of procedures, relaxed welcoming atmosphere, confident professional manner
b) Education, relaxation techniques, Desensitisation (graded exposure to stimulus), short term pharmacological anxiolytics e.g. diazepam, long term pharmacological antidepressants

100
Q

In obsessive compulsive disorder, what are the obsessions and what are the compulsions?

A

Obsessions = recurrent, intrusive and depressive thoughts or impulses - egodystonic (goes against pts wishes) - pt tries to supress

Compulsions = motor response to obsessions, ritualised behaviour, resisted until anxiety unbearable, behaviour performed and reinforced

101
Q

What is hypochondriasis?

A

Abnormal preoccupation with health or bodily functions. Focus of distress on belief of presences of underlying physical disease, not the symptoms i.e. abnormal interpretation of normal sensations

102
Q

What is the management of hypochondriasis?

A

Early and reliable diagnosis ruling out physical cause, psychiatric help with behavioural and cognitive technique, treat underlying mental illnesses

103
Q

What is phychogenic pain?

A

Pain caused phychologically rather than organic/physically. Effectively a somatoform disorder but different to hypochondrias.

104
Q

How is phychogenic pain diagnosed?

A
  • Inconsistent with known anatomical landmarks ie different nerves involved
  • Associated with preventing sleep but bt doesn’t wake up from it
  • Analgesics ineffective
  • Associated with emotional factors
  • Continuous and may be bilateral
  • Repeated negative investigations
105
Q

What is anorexia nervosa?

A

Body weight 15% below normal, restrict food intake, amenorrhea (period stops)

106
Q

What is the lifetime risk of schizophrenia and when is age of onset?

A
  • 1% F=M

- Mid adulthood F=32 yrs, M=28 yrs

107
Q

What is the management of schizophrenia?

A

Meds e.g. clozapine, typical/atypical neuroleptics

Physchoeducation, CBT and family therapy

108
Q

What are affective disorders?

A

Extremes of mood, if accompanied by assicated symptoms and impaired function can be delinaiated into illness e.g bipolar

109
Q

What is the course of depression?

A
  • 80-90% recover with Tx
  • Episodes are toxic and can reoccur
  • Chronic depression and Tx resistance depression
  • Dysthemia = long standing
110
Q

In the management of depression, what is primary care and what is secondary care?

A 
Primary = antidepressants, counselling, social intervention 
Secondary = med review, therapy, community support team
111
Q

What features of mania (elated or irritable mood for more than 1 week) are there?

A
  • Disinhibition
  • Reduced need for sleep
  • Inflated self-esteem
  • Delusions
  • Racing thoughts
  • Rapid loud speech
  • Risk taking activity
  • Overactivity
  • Distractibility
  • Hallucination
112
Q

What questionaire is used for alcoholism?

A

CAGE
C= feel you should cut down?
A = annoyed if people comment on drinking?
G= guilty about amount drink?
E= every drunk early morning as eye opener?

113
Q

What is the role of the thalamus?

A

Relay station for impulses arriving from brainstem, regulates sleep

114
Q

What is the role of the hypothalamus?

A

Responsible for hormone production, body temperature, thirst and hunger

115
Q

What is the role of the occipital lobe and the temporal lobe?

A 
Occipital = processes visual information 
Temporal = regulates memory, hearing, language and learning
116
Q

What is the role of the cerbellum?

A

Maintains posture balance and movement

117
Q

What is the role of the parietal lobe and frontal lobe?

A 
Parietal = compiles sensory info from all over body, words into thoughts 
Frontal = decision making, consciousness, problem solving
118
Q

What are the positive neurotransmitters?

A
  • Adrenaline
  • Noradrenaline
  • Dopamine
119
Q

What are the negative neurotransmitters?

A
  • Seratonin
  • GABA
  • Dopamine
120
Q

What are the functions of NT seratonin? Where does it act?

A
  • Mood
  • Memory processing
  • Sleep
  • Cognition
  • Pain
    Acts all over cerebral cortex
121
Q

What are the functions of NT dopamine? Where does it act?

A
  • Motor function (fine tuning)
  • Reward (motivation)
  • Perseveration
  • Compulsion
  • Pleasure, euphoria
  • Pain
    Acts via 4 pathways, principally on frontal cortex
122
Q

What are the functions of NT noradrenaline? Where does it act?

A
  • Mediates arousal ready for fight or flight
  • Vigilance
  • Pain
    Acts all over and very specific to sympathetic nervous system
123
Q

What first line anticonvulsants are used in tonic-clonic seizures? In focal seizures?

A

Sodium valproate and iamotrigene

Carbamazepine and iamotrigene

124
Q

What are the two main methods that anticonvulsant drugs use to inhibit the repetitive firing?

A

1) Inhibition of ionic channels such as Na or Ca - phenytoin or carbamazepine
2) Enhance GABA mediated inhibition of brain and neurones to decrease excitatory transmission. BZD = potentiate Cl through GABA channel. Vigabatrin = inhibit GABA degredation. Gabapentin = acts as GABA agonist

125
Q

Which 4 anticonvulsant drugs decrease glutamate neurotransmission (excitatory in epilepsy and pain)?

A

Phenytoin, Lamotrigine, Gabapentin, Iamotrigine

126
Q

What are the 5 MOA that anticonvulsants use in stopping neuropathic pain?

A

1) Decrease neurogenic inflammation thats driven by neuropeptides e.g. CGRP and Substance P (source of phantom tooth pain)
2) Stabilise membranes by inhibiting ion channels
3) Enhance anti-nociceptive mechanisms by acting as GABA analogue
4) Decrease trigeminal activation
5) Modulate CNS effects

127
Q

In status epilepticus, what medication should be given?

A

Midazolam:
Buccally (Buccolam)- for adults 10mg in 1ml syrup, pre-filled syringes for age, repeat once after 10 mins if no response
IV and IM - 5 mg

128
Q

Why are benzodiazepines not used as a 1st line anticonvulsant drug?

A

Dependence risk - only used in status epilepticus

129
Q

What is the 1st line medication used for trigeminal neuralgia?

A

Carbamazepine

130
Q

What are the side effects of taking carbamazepine for trigeminal neuralgia?

A
  • Steven-Johnsons syndrome (widespread mucotaneous reaction)
  • Blood dyscrasias (haemolytic anaemia, thrombocytopenia, bruising)
  • Liver disorders (yellowing of skin, malaise)
131
Q

What is the important genetic variation in the pharmacological response to carbamazepine that may make the pt more prone to Steven Johnsons syndrome?

A

HLA-B*1502 allele - ancestry across broad areas of Asia

132
Q

What are the contraindications for taking carbamazepine?

A
  • AV conduction abnormalities
  • Bone marrow depression
  • Liver disease
133
Q

What is the regimen for carbamazepine and what should be monitored?

A

100-200mg once daily increaseing slowly to TDS
Max 1600mg total daily
Monitor with FBC, U+E, LFT every 6 weeks then every 3-6 months

134
Q

How do anticonvulsants impact on dental treatment?

a) Carbamazepine
b) Phenytoin

A

Both: Haematological effects (anaemia, white cells, platelets) so ask if blood tests normal, hepatic enzyme inducers so be wary of drug interactions

a) xerostomia, glossitis, oral ulceration, cleft lip and palate, cervical lymphadenopathy
b) Gingival overgrowth, cleft lip and palate (teratogenic effect), root shortening and/or resorption, hypercementosis, salivary gland hypertrophy, cervical lymphadenopathy

135
Q

What are the 4 major pathways for dopamine?

A
  • Mesiolimbic = rewards and reinforcement
  • Mesiocortical = emotional response and motivation
  • Tubero-infundibular = hormone
  • Nigostriatial = movement (primary pathway affected in Parkinsons)
136
Q

What neurotransmitter increases and which decreases in Parkinsons?

A

Increased acetylcholine, decreased dopamine

137
Q

What are the 3 ways of increasing dopamine through dopaminergic medications?

A

1) Precursor of dopamine
2) Decrease dopamine metabolism centrally or peripherally
3) Direct dopamine synthetic agonists to stimulate dopamine release

138
Q

For precursor of dopamine:

a) Why is this used
b) What precursor?
c) Where does Levadopa act?
d) Why is increased frequency of administration required?

A

a) Dopamine doesn’t cross BBB
b) L-Dopa
c) 1-2% crosses BBB, remainder converted in gut and liver through decarboxylation which acts peripherally
d) Decreases in effectiveness over time

139
Q

For decreasing dopamine metabolism peripherally:

a) Why do we want to stop the metabolism of levadopa to dopamine?
b) What peripheral blocks are packaged into Levadopa?
c) What enzyme is also in the peripheries that can metabolise levadopa?
d) What drugs are COMT inhibitors?

A

a) Dopamine doesnt cross BB so increases circulating levadopa which can cross BBB
b) Benserazide (co-benlodopa), Carbidopa (co-carbidopa)
c) COMT
d) Entacapone, Tolcapone

140
Q

For decreasing dopamine metabolism centrally:

a) In a centralized block, what are the drugs given?
b) How do these help?

A

a) Monoamine oxidase B inhibitors (MAOB inhibitors)
b) Dopamine isn’t broken down as much so can decrease the dose of Levadopa needed or increase the time it exerts its effects

141
Q

For direct dopamine synthetic agonists:

a) What do they do?
b) What are the side effects?

A

a) Stimulate the remaining dopamine system to produce dopamine by binding to dopaminergic receptors
b) Cause compulsive and impulsive behavioural changes

142
Q

What is the relevance of antiparkinsonian medications to dentistry?

A
  • Dry mouth
  • Taste disturbances
  • Difficulty tolerating dentures
  • Stomatitis
  • Oral ulceration
  • Burning mouth sensation
  • Dysphagia and chewing difficulties
  • Hypersalivation from acetylcholine
  • Dyskinesia (unusual movements)
143
Q

What drugs interact with the following antiparkinsonian medications that you can prescribe as a dentist:

a) Levadopa
b) Bromocriptine
c) Entacapone
d) Selegeline

A

a) Antagonised by BZD
b) Erythromycin increases toxicity
c) Reduce adrenaline dose
d) Avoid opioids as CNS toxicity

144
Q

Anti-muscarinic drugs can be given to parkinsons pts to reduce the effects of central cholinergic excess: Orphenadrine, procyclidine, trihexphenidyl. What is a side effect of these relevant to dentistry?

A

Dry mouth

145
Q

When treating a parkinsons patient what should you ask and when should you treat them?

A

When ‘ON’ time is i.e. when meds are working - usually within 60-90 mins of taking

Often morning appts better and short

146
Q

For Antipsychotics,

a) Where are they metabolised
b) What do they bind to
c) they are hepatic enzyme inducers, what does this mean?

A

a) Liver - high plasma protein binding so greater risk of drug interactions and high first pass metabolism
b) Non-specific binding to adrenergic receptors and cholinergic receptors (sedative effects)
c) High chance of drug interactions, preferentially metabolise drug

147
Q

For the MOA of Antipsychotics, what do they do?

A

Don’t treat psychosis but decrease the positive symptoms gradually by decreasing dopaminergic neurotransmission

148
Q

What are the 1st generation antipsychotics and what are they used for?

A

Chlorpromazine - used for anti-nausea

Haloperidol - not routine but if severely distressed

149
Q

What are the 2nd generation antipsychotics and what are their advantages and drawbacks?

A

Olanzipine and Risperidone

Lower risk of side effects but arguements over effects on cognitive ability

150
Q

What are the adverse effects of antipsychotics?

A

Extrapyramidal A.E:

  • Parkinsonian symptoms
  • Dystonia (abnormal face and body movements)
  • Akathisia (restlessness)
  • Tardive dyskinesia (rhythmic involuntary movement of tongue face and jaw)

Neuroleptic malignant syndrome (fever, muscular rigidity, autonomic dysfunction)

Prolactin secretion (breast in male and female)

151
Q

What drugs that dentist can prescribe interact with antipsychotics?

A
  • Erythromycin = ventricular arrythmias
  • TCA and some SSRIs = ventricular arrythmias
  • Tramadol = increased risk convulsions
  • Alcohol and anxiolytics = increased sedation
152
Q

What side effects relevant to dentistry does Chlorpromazine have?

A
  • Xerostomia, decreased sweating and constipation - through antagonism of muscarinic receptors
  • Sedation - through antagonism of histamine H1 receptors
153
Q

What side effect relevant to dentistry does Chlorpromazine, Haloperidol and Risperidone have?

A

Postural hypotension

154
Q

What NICE guidelines are available on Depression?

A

CG 90 - Depression in adults 2009

CG 91 - Depression in adults with chronic physical health problem 2009

155
Q

In depression, for which group is low intensity psychosocial interventions key priority?

A

Subthreshold mild - mod depressives

156
Q

In depression, for which group is pharmacological management indicated? What is the first choice of drug?

A
  • Subthreshold persistent >2years
  • Mild with chronic physical health problems
  • Unresponsive to low level intervention
  • Mod-sever depression along with high intensity psychosocial intervention

SSRI first choice

157
Q

What has been hypothesised for causing depression?

A
  • Monoamine deficiency e.g. dopamine, serotinine, noradrenaline
  • Neurotrophic - loss of neurotrophic support, lack of nerve growth factors for resilience and neurogenesis
158
Q

What group of antidepressant drugs are Fluoxetine, Citalopram and Parxetine?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)

159
Q

What group of antidepressant drugs are Duloxetine and Venlafaxine?

A

Selective Noradrenaline Reuptake Inhibitors (SNRIs)

160
Q

What group of antidepressant drugs are Amitriptyline and Nortriptyline?

A

Tricyclic antidepressants (TCAs)

161
Q

What group of antidepressant drugs is Phenelzine?

A

Monoamine Oxidase Inhibitors (MAOIs)

162
Q

What is the MOA of SSRIs?

A

Increase the extracellular levels of 5HT by inhibiting the reuptake into the presynaptic cell so more binds to the postsynaptic cell. Enhances neuronal plasticity and improves emotional bias

163
Q

What are the unwanted effects of SSRIs?

A 
Less sedative but still are 
Nausea and vomiting 
GI disturbance 
Disrupts sleep 
Dizziness 
Can cause bruxism in minority (3.2%)
164
Q

When are SNRIs given?

A

3rd line drug in depression and 3rd line drug in neuropathic pain (NICE)

165
Q

What are the unwanted effects of SNRIs?

A

Nausea and vomiting
Sexual dysfunction
Cardiovascular effects - prolonged QT interval and Hypertension
Rarely but hepatic damage

166
Q

What is the MOA of TCAs (remember ‘dirty’)

A

Non selective block of monoamine uptake (5HT and Nadr)
Antihistaminergic activity causing sedation
Block Na, K and Ca channels
Weak NDMA antagonist
Enhance GABA peripherally

167
Q

Why are TCAs no longer first choice for depression?

A

Unwanted side effect profile - postural hypertension, prolong QT interval, sedating, xerostomia, blurred vision, increased ocular pressure
Dangerous in overdose - acidosis difficult to reverse
2-3 week window before effective

168
Q

What are TCAs good for?

A

Chronic pain

169
Q

What is the MOA of MAOIs?

A

Blocks monoamine oxidase enzymes that degrade monoamine, increasing monoamine levels

170
Q

Why does an MAOI crisis (hypertension and severe headache) occur a patient eats cheese?

A

GIT has a lot on monoamine oxidase enzymes, which are then blocked. Amines absorbed more from tyramine rich cheese.

171
Q

What are the unwanted effects of MAOIs?

A

Postural hypotension
Xerostomia
Multiple drug interactions - other CNS depressants can cause coma

172
Q

Why should you think twice if you are prescribing antidepressents to the following patients:

a) Cardiovascular disease
b) Diabetic
c) Epileptic

A

a) prolong QT interval
b) affects glycaemic control through affects on alpha-adrenoreceptors
c) Decreases seizure thresholds

Human Diseases Yr4 (10 decks)

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