Neurological disorders Flashcards
(172 cards)
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)
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
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.
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
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.
6
Q
What is a Stokes-Adams Attack?
A
Result of cardiac arrythmias, often no warning or palpitations, drop attacks - LOC
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)
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
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.
10
Q
What treatment is given for multiple sclerosis which can help long term prognosis?
A
Steroids
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
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
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
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
15
Q
Are brain tumours more common as primary or metastases?
A
Metastases - from lung, breast, GIT and kidney
16
Q
What is Eaton-Lambert syndrome?
A
Seen in patients with lung/other cancers where muscles get stronger rather than weaker with activity
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
18
Q
What long term drug use can cause tics/ involuntary facial movements?
A
Phenothiazine
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.
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
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)
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
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
24
Q
What is cerebral palsy?
A
Disorder of motor function secondary to cerebral damage - frequently associated with birth injury or hypoxia
25
What is spina bifida?
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)
26
What are 2 distinct clinical features of spina bifida?
- Tuft of hair at base of spine
- Meningocele - where meningeal layer surrounding spinal cord herniates out between the bones of vertebrae (usually lumbar)
27
What is Huntington's Chorea?
Progressive dementia with marked involuntary movements. Autosomal dominant and early onset of middle age.
28
What is a stroke?
Sudden focal loss of neurological function due to disruption of blood supply to part of the brain - permanent damage and disabling
29
What are the 2 main pathophysiologies/causes of a stroke?
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%)
30
How can you tell if there has been a cerebral haemorrhage from a CT scan?
White - RBC have iron which absorb x rays
31
How can you tell if there has been an ischaemic stroke from a CT scan a)mild b) severe?
a) Subtle changes e.g. sulci on brain less visible
| b) Dark from infarction
32
What are the risk factors of a stroke?
- Age
- Smoking
- Diabetes
- Hypertension
- Coagulation disorders
- Atrial fibrillation
- Hyperlipidaemia
33
What measures can be taken to prevent strokes?
- 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
34
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) Total anterior circulation stroke
b) Partial anterior circulation stroke
c) Lacuna stroke
d) Posterior circulation stroke
35
What test is used in hospitals to recognise stroke? What test do members of the public use?
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
36
Once a patient is in hospital, what is the acute stroke management?
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
37
What is a transient ischaemic attack (TIA)?
Transient focal neurological deficit lasting less than 24 hours, usually less than an hour
38
What do the following mean?
a) Dysarthria
b) Dysphonia
c) Dysphasia - expressive and receptive
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
39
What are the 3 phases of swallowing and which phases does a stroke affect?
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
40
What are some causes of dysphagia?
- 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
41
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) SALT and videofluoroscopy (swallowing Xray)
b) Barium swallow
c) Barium swallow or endoscopy
d) Endoscopic biopsy, CT scan
42
What is offered in the following treatments
a) Neurological
b) Mechanical
c) Diet modification
d) Tube feeding
a) SALT
b) Dilation, stent, surgery
c) Puree
d) nasogastric, PEG feeding (percutaneous endoscopic gastrocopy endoscope through abdominal wall into stomach)
43
What compensatory mechanisms are part of intracranial pressure autoregulation?
- Decreasing the production of CSF
| - Restricting blood flow to brain by vasoconstriction
44
What are the indications of a head injury?
- 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
45
What should you do if there has been a scalp injury?
- Bleeds profusely so apply direct pressure
46
What are skull injuries divided into?
- Open skull fractures (compound fracture)
- Closed skull fracture
- Basal skull fracture
47
What is a primary (direct) brain injury?
Occurs at time of original insult, direct damage to prain parenchyma and associated with vascular injuries
48
What is a primary (direct) brain injury?
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.
49
What is a secondary brain injury?
Damage after initial insult. Expanding mass lesions, swelling, bleeding quickly. Increased intracranial pressure or brain herniation
50
What is a concussion?
Transient alteration in neurological function. Mild injury from blunt trauma with no detectable brain damage but short term memory loss
51
What is a contusion?
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)
52
What is a diffuse axonal injury?
Rotational forces on the brain causing snapping and stretching of axons. Disturbance can produce temporary or widespread damage, coma or death.
53
What is a sub-dural haemotoma?
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.
54
What is an extra-dural haematoma?
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
55
What is an intracerebral haematoma?
Blood within the brain parenchyma
56
What are the symptoms of an early intracranial haemorrhage?
- Nausea
- Severe head pains
- Dizziness
- Sleepiness
- Unequal pupil size
57
What are the symptoms of late intracranial haemorrhage?
- Convulsions
- Deteriorating consciousness
- Increased BP
- Slow pulse
- Slow respiration
- Neck rigidity
58
What imaging techniques are used in a brain injury?
X-rays - show bone only
| CT and MRI - show more anatomy and density of blood
59
What are the layers of the brain outer to inner?
Skull - dura mater - arachnoid mater - subarachnoid space - pia mater - brain
60
What is the management of a patient presenting with a head injury?
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)
61
What is GCS?
Eye opening response up to 4 points, verbal response up to 5 points, motor response up to 6 points.
3=comatosed, 15= fully alert
62
What is a subarachnoid haemorrhage? What causes this?
Bleeding beneath the arachnoid membrane
| Burst cerebral aneurysms
63
What does ACVPU stand for?
- Alert
- New onset confusion
- Responds to voice
- Responds to pain
- Unresponsive
64
Define these words: a) Catelepsy b) Ambivalence c) Psychosis d) Dementia e) Neurosis
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
65
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 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
66
What are the complications of alcoholism?
- Injuries
- Nutritional defects
- Brain damage, epilepsy and myopathy
- Cardiomyopathies
- Gastritis
- Pancreatitis
- Liver damage
- Social problems
67
What is Korsakoff's Psychosis?
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)
68
What are the medical complications of bulimia?
- Dehydration/weight fluctuations
- Low potassium causing muscle cramps
- Dental erosion
- Acidosis/alkylosis
- Oesophagitis
- Poor muscular tone in colon from laxative abuse
69
What signs should you look for if you suspect self-induced vomiting?
- Calluses on back of finger (Russel sign)
- Traumatic lesions on back of palate
- Dental erosion
70
Define the following: a) Obsessive-compulsive b) Paranoia c) Sociopathy d) Dependency e) Somatoform disorder
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
What are the common symptoms of schizophrenia?
- 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
What should you look out for is you suspect a pt has body dysmorphic disorder?
- 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
What are the uses of hypnotic drugs?
| What are the 4 classifications of hypnotic drugs?
- Before surgery, during a life crisis (short term), supplement to pain control
- Benzodiazepines, antihistamines, miscellaneous, barbiturates
74
What does physiologic sleep comprise of?
75% non-rapid eye movement (NREM)
| 25% rapid eye movement (REM)
75
What are the sleep phases in NREM?
```
N1 = light sleep
N2 = asleep
N3= Best sleep - muscles relax, energy restored, BP, RR decrease
N4 = delta wave
```
76
What occurs in REM sleep?
Dreaming, body relaxed and immobile. Provides energy and supports daytime performance
77
What occurs in drug induced sleep?
Increased NREM, decreased REM
78
What are the effects of Benzodiazepines?
- 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
What BZD drugs are used as hypnotics for
a) initial insomnia
b) early morning wakening
a) Tamazepam, Loprazolam = shorter time, less hangover
| b) Nitrazepam = longer acting
80
How should pts be withdrawn from BZD?
Slowly to avoid rebound insomnia and anxiety, worst after acute withdrawal of short acting drugs
81
What is the site of action for Benzodiazepines?
- Reticular activating system = controls conscious, alert state (hypnotic effect)
- Limbic system in cortex = controls emotion (anxiolytic effect)
82
What is the MOA for Benzodiazepines?
Influence GABA at chloride channel to increase frequency of channel opening
83
What drug is used to reverse the affects of BZD and Z drugs?
Flumazenil - antagonist with stronger binding but induces seizures so use carefully
84
How are antihistamines used as hypnotics?
H1 blockers produce CNS depression at therapeutic doses. Promethazine used in children
85
What are the Z drugs used for insomnia and are less likely to become dependent on than BZD?
Zolpidem and Zopiclone
86
What are the uses of anxiolytics (sedatives)?
| What are the drugs that have anxiolytic effects?
- Pre-med, sedation, muscle relaxants e.g. TMD and dislocation, emergency drugs e.g. epilepsy, amnesic effect
- Alcohol, BZD. Buspirone, Beta-adrenergic blockers
87
In alcohol consumption, how long does it take to reach peak plasma levels and how long until sedation? How are patients withdrawn?
30 mins, 60 mins
| Decreasing dose of sedative. Chlordiazepoxide used (BZD)
88
Which two BZD are in the Dental formulary and what is the max no of days it can be prescribed for?
Diazepam (for short term muscle relaxant) and Temazepam
| 5 Days
89
What is Buspirone? What are its effects?
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
What are beta-blockers used for?
Treating somatic anxiety e.g. tremor, palpitations = propanalol. Doesn't stop anxiety feeling just symptoms. Not used in dental pts
91
What drug is the 'gold standard' anxiolytic?
Benzodiazepines
92
The international classification of disease version 10 outlines what categories for mental health disorders?
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
When is anxiety deemed as pathological?
When the feeling becomes to intense, frequent or persistent and interferes with functioning of the individual.
94
What are the psychological and physical symptoms of anxiety?
```
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
What is generalised anxiety disorder?
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
What are panic attacks?
Anxiety so intense theres an overwhelming feeling of panic, identifiable trigger, short lived, feels like having heart attack
97
Define phobia
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
What cycle increases the likelihood of anxiety being experienced in similar situations and increases the chance of further avoidance?
'Avoidance/relief'
99
How can you manage dental anxiety through a) preventing it b) treating it?
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
In obsessive compulsive disorder, what are the obsessions and what are the compulsions?
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
What is hypochondriasis?
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
What is the management of hypochondriasis?
Early and reliable diagnosis ruling out physical cause, psychiatric help with behavioural and cognitive technique, treat underlying mental illnesses
103
What is phychogenic pain?
Pain caused phychologically rather than organic/physically. Effectively a somatoform disorder but different to hypochondrias.
104
How is phychogenic pain diagnosed?
- 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
What is anorexia nervosa?
Body weight 15% below normal, restrict food intake, amenorrhea (period stops)
106
What is the lifetime risk of schizophrenia and when is age of onset?
- 1% F=M
| - Mid adulthood F=32 yrs, M=28 yrs
107
What is the management of schizophrenia?
Meds e.g. clozapine, typical/atypical neuroleptics
| Physchoeducation, CBT and family therapy
108
What are affective disorders?
Extremes of mood, if accompanied by assicated symptoms and impaired function can be delinaiated into illness e.g bipolar
109
What is the course of depression?
- 80-90% recover with Tx
- Episodes are toxic and can reoccur
- Chronic depression and Tx resistance depression
- Dysthemia = long standing
110
In the management of depression, what is primary care and what is secondary care?
```
Primary = antidepressants, counselling, social intervention
Secondary = med review, therapy, community support team
```
111
What features of mania (elated or irritable mood for more than 1 week) are there?
- Disinhibition
- Reduced need for sleep
- Inflated self-esteem
- Delusions
- Racing thoughts
- Rapid loud speech
- Risk taking activity
- Overactivity
- Distractibility
- Hallucination
112
What questionaire is used for alcoholism?
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
What is the role of the thalamus?
Relay station for impulses arriving from brainstem, regulates sleep
114
What is the role of the hypothalamus?
Responsible for hormone production, body temperature, thirst and hunger
115
What is the role of the occipital lobe and the temporal lobe?
```
Occipital = processes visual information
Temporal = regulates memory, hearing, language and learning
```
116
What is the role of the cerbellum?
Maintains posture balance and movement
117
What is the role of the parietal lobe and frontal lobe?
```
Parietal = compiles sensory info from all over body, words into thoughts
Frontal = decision making, consciousness, problem solving
```
118
What are the positive neurotransmitters?
- Adrenaline
- Noradrenaline
- Dopamine
119
What are the negative neurotransmitters?
- Seratonin
- GABA
- Dopamine
120
What are the functions of NT seratonin? Where does it act?
- Mood
- Memory processing
- Sleep
- Cognition
- Pain
Acts all over cerebral cortex
121
What are the functions of NT dopamine? Where does it act?
- Motor function (fine tuning)
- Reward (motivation)
- Perseveration
- Compulsion
- Pleasure, euphoria
- Pain
Acts via 4 pathways, principally on frontal cortex
122
What are the functions of NT noradrenaline? Where does it act?
- Mediates arousal ready for fight or flight
- Vigilance
- Pain
Acts all over and very specific to sympathetic nervous system
123
What first line anticonvulsants are used in tonic-clonic seizures? In focal seizures?
Sodium valproate and iamotrigene
| Carbamazepine and iamotrigene
124
What are the two main methods that anticonvulsant drugs use to inhibit the repetitive firing?
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
Which 4 anticonvulsant drugs decrease glutamate neurotransmission (excitatory in epilepsy and pain)?
Phenytoin, Lamotrigine, Gabapentin, Iamotrigine
126
What are the 5 MOA that anticonvulsants use in stopping neuropathic pain?
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
In status epilepticus, what medication should be given?
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
Why are benzodiazepines not used as a 1st line anticonvulsant drug?
Dependence risk - only used in status epilepticus
129
What is the 1st line medication used for trigeminal neuralgia?
Carbamazepine
130
What are the side effects of taking carbamazepine for trigeminal neuralgia?
- Steven-Johnsons syndrome (widespread mucotaneous reaction)
- Blood dyscrasias (haemolytic anaemia, thrombocytopenia, bruising)
- Liver disorders (yellowing of skin, malaise)
131
What is the important genetic variation in the pharmacological response to carbamazepine that may make the pt more prone to Steven Johnsons syndrome?
HLA-B*1502 allele - ancestry across broad areas of Asia
132
What are the contraindications for taking carbamazepine?
- AV conduction abnormalities
- Bone marrow depression
- Liver disease
133
What is the regimen for carbamazepine and what should be monitored?
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
How do anticonvulsants impact on dental treatment?
a) Carbamazepine
b) Phenytoin
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
What are the 4 major pathways for dopamine?
- Mesiolimbic = rewards and reinforcement
- Mesiocortical = emotional response and motivation
- Tubero-infundibular = hormone
- Nigostriatial = movement (primary pathway affected in Parkinsons)
136
What neurotransmitter increases and which decreases in Parkinsons?
Increased acetylcholine, decreased dopamine
137
What are the 3 ways of increasing dopamine through dopaminergic medications?
1) Precursor of dopamine
2) Decrease dopamine metabolism centrally or peripherally
3) Direct dopamine synthetic agonists to stimulate dopamine release
138
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) 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
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) 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
For decreasing dopamine metabolism centrally:
a) In a centralized block, what are the drugs given?
b) How do these help?
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
For direct dopamine synthetic agonists:
a) What do they do?
b) What are the side effects?
a) Stimulate the remaining dopamine system to produce dopamine by binding to dopaminergic receptors
b) Cause compulsive and impulsive behavioural changes
142
What is the relevance of antiparkinsonian medications to dentistry?
- Dry mouth
- Taste disturbances
- Difficulty tolerating dentures
- Stomatitis
- Oral ulceration
- Burning mouth sensation
- Dysphagia and chewing difficulties
- Hypersalivation from acetylcholine
- Dyskinesia (unusual movements)
143
What drugs interact with the following antiparkinsonian medications that you can prescribe as a dentist:
a) Levadopa
b) Bromocriptine
c) Entacapone
d) Selegeline
a) Antagonised by BZD
b) Erythromycin increases toxicity
c) Reduce adrenaline dose
d) Avoid opioids as CNS toxicity
144
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?
Dry mouth
145
When treating a parkinsons patient what should you ask and when should you treat them?
When 'ON' time is i.e. when meds are working - usually within 60-90 mins of taking
Often morning appts better and short
146
For Antipsychotics,
a) Where are they metabolised
b) What do they bind to
c) they are hepatic enzyme inducers, what does this mean?
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
For the MOA of Antipsychotics, what do they do?
Don't treat psychosis but decrease the positive symptoms gradually by decreasing dopaminergic neurotransmission
148
What are the 1st generation antipsychotics and what are they used for?
Chlorpromazine - used for anti-nausea
| Haloperidol - not routine but if severely distressed
149
What are the 2nd generation antipsychotics and what are their advantages and drawbacks?
Olanzipine and Risperidone
| Lower risk of side effects but arguements over effects on cognitive ability
150
What are the adverse effects of antipsychotics?
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
What drugs that dentist can prescribe interact with antipsychotics?
- Erythromycin = ventricular arrythmias
- TCA and some SSRIs = ventricular arrythmias
- Tramadol = increased risk convulsions
- Alcohol and anxiolytics = increased sedation
152
What side effects relevant to dentistry does Chlorpromazine have?
- Xerostomia, decreased sweating and constipation - through antagonism of muscarinic receptors
- Sedation - through antagonism of histamine H1 receptors
153
What side effect relevant to dentistry does Chlorpromazine, Haloperidol and Risperidone have?
Postural hypotension
154
What NICE guidelines are available on Depression?
CG 90 - Depression in adults 2009
| CG 91 - Depression in adults with chronic physical health problem 2009
155
In depression, for which group is low intensity psychosocial interventions key priority?
Subthreshold mild - mod depressives
156
In depression, for which group is pharmacological management indicated? What is the first choice of drug?
- 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
What has been hypothesised for causing depression?
- Monoamine deficiency e.g. dopamine, serotinine, noradrenaline
- Neurotrophic - loss of neurotrophic support, lack of nerve growth factors for resilience and neurogenesis
158
What group of antidepressant drugs are Fluoxetine, Citalopram and Parxetine?
Selective Serotonin Reuptake Inhibitors (SSRIs)
159
What group of antidepressant drugs are Duloxetine and Venlafaxine?
Selective Noradrenaline Reuptake Inhibitors (SNRIs)
160
What group of antidepressant drugs are Amitriptyline and Nortriptyline?
Tricyclic antidepressants (TCAs)
161
What group of antidepressant drugs is Phenelzine?
Monoamine Oxidase Inhibitors (MAOIs)
162
What is the MOA of SSRIs?
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
What are the unwanted effects of SSRIs?
```
Less sedative but still are
Nausea and vomiting
GI disturbance
Disrupts sleep
Dizziness
Can cause bruxism in minority (3.2%)
```
164
When are SNRIs given?
3rd line drug in depression and 3rd line drug in neuropathic pain (NICE)
165
What are the unwanted effects of SNRIs?
Nausea and vomiting
Sexual dysfunction
Cardiovascular effects - prolonged QT interval and Hypertension
Rarely but hepatic damage
166
What is the MOA of TCAs (remember 'dirty')
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
Why are TCAs no longer first choice for depression?
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
What are TCAs good for?
Chronic pain
169
What is the MOA of MAOIs?
Blocks monoamine oxidase enzymes that degrade monoamine, increasing monoamine levels
170
Why does an MAOI crisis (hypertension and severe headache) occur a patient eats cheese?
GIT has a lot on monoamine oxidase enzymes, which are then blocked. Amines absorbed more from tyramine rich cheese.
171
What are the unwanted effects of MAOIs?
Postural hypotension
Xerostomia
Multiple drug interactions - other CNS depressants can cause coma
172
Why should you think twice if you are prescribing antidepressents to the following patients:
a) Cardiovascular disease
b) Diabetic
c) Epileptic
a) prolong QT interval
b) affects glycaemic control through affects on alpha-adrenoreceptors
c) Decreases seizure thresholds
