Brainscape's Knowledge GenomeTM

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


See full index

4TH YEAR - CPTP > Week 3 - PD & E > Flashcards

Week 3 - PD & E Flashcards

1
Q

What are the cardinal signs of PD?

A

BRADYKINESIA
+ 1 of:
Rigidity, Tremor or Postural Instability

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

What is the pathophysiology of PD?

A

Loss of dopaminergic cells in substantia nigra&raquo_space;> degeneration of projections to other areas of basal ganglia

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

What is the protein found in lewy bodies?

A

Alpha-synuclein

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

What is the site of action of Levodopa?

A

Increases L-Dopa levels in the presynaptic cleft

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

What is the site of action of Dopamine Agonists?

A

Act directly on postsynaptic dopamine receptors in striatum (D1 and/or D2)

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

What is the site of action of Amantadine (antiviral)?

A

Stimulates release of DA and inhibits re-uptake at the pre-synaptic cleft

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

What is the site of action of COMT inhibitors (catechol-O-methyltransferase) such as Entacapone or Tolcapone?

A

Block degradation of DA and L-Dopa in the synapse (prolong effect)

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

What is the site of action of MAOIs (Monoamine-oxidase-B inhibitors) such as Selegiline & Rasagiline?

A

Irreversible inhibitors of MAOB which decreases break down of DA&raquo_space;> which leaves more in the synapse.

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

Where is levodopa absorbed?

A

Small bowel via AA transport system

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

What is the half life of levodopa?

A

~60 mins

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

What are the short term side effects of levodopa?

A

N&V, reduced appetite, confusion, delusions, visual hallucinations, postural hypotension, insomnia, vivid dreams/nightmares

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

What are the long term side effects of levodopa?

A

Dyskinesias (abnormal involuntary movemnets), Confusion,
Hallucinations
Response fluctuations (end of dose deterioration and unpredictable on-off switching)

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

Name 3 dopamine agonists…

A

Ropinirole, Pramipexole, Rotigotine, Apomorphine

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

How can dopamine agonists be administered?

A

Oral, transdermal (Rotigotine) or subcutaneous (Apo) administration

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

What are the common side effects of dopamine agonists?

A

N&V, loss of appetite, postural hypotension, confusion, hallucinations, somnolence and

Impulse control disorder (gambling, hypersexuality, over spending etc. prewarn patient and family)

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

What are the side effects of MAOIs?

A

Nausea, vomiting, confusion

There is a potential interaction with anti-depressants (SSRIs) → serotonin syndrome

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

Name 2 MAOIs…

A

Selegiline, Rasagiline

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

Why do you use COMT inhibitors?

A

Inhibit COMT → more LD available to cross the BBB to produce prolonged effect

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

What are the side effects of COMT inhibitors?

A

N&V, Confusion etc. +

Increased dyskinesias, diarrhoea and discolouration of body fluids

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

When do you use amantadine?

A

Largely used in later disease to treat dyskinesia

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

What are the s/e of amantadine?

A

Confusion (do not use in elderly), Hallucinations, psychosis, Livedo reticularis, ankle oedema

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

When do you use anticholinergics?

How do they work?

A

Used more in younger patients with tremor

Reduce effects of relative central ACh excess that occurs due to dopaminergic deficiency

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

What are the side effects of anticholinergics?

A

Cognitive impairment (in elderly)

Dry mouth, constipation, dizziness, blurred vision, urinary retention, glaucoma

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

What non-dopamine related treatments may be used?

A

Always remember PD patients have non neuro symptoms such as nocturia, urgency, constipation, depression, anxiety etc. All of which will need addressing.

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

What are the 2 mechanisms of underlying seizures?

A

Excess excitation – of inward Na+, Ca++ currents or too many neurotransmitters such as: glutamate, aspartate

Inadequate inhibition – Of inward Cl- and outward K+ currents or not enough of the neurotransmitter GABA

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

What are the possible prophylactic measures taken with epileptic patients?

A

Prophylactic measures include ways of minimising epileptogenic stimuli such as:

Fever, flicking lights, loss of sleep, alcohol abuse (induced and withdrawal), abrupt withdrawal of medication and certain epileptogenic drugs such as antibiotics.

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

What is the 1st line treatment in generalised tonic clonic seizures?

A

Sodium valproate

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

When can you not use sodium valproate?

A

Pregnancy - teatrogenic

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

What are the alternatives to sodium valproate in the management of generalised tonic clonic seizures?

A

lamotrigine if sodium valproate unsuitable (women)– but may exacerbate myoclonus).

Also consider carbamazepine or oxcarbazepine (may exacerbate myoclonus)

30
Q

When can you not use carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabalin, tiagabine or vigabatrin?

A

In presence of myoclonus or absences

31
Q

What is the 1st line treatment in absence seizures?

A

Ethosuximide (absences only) or valproate

Lamotrigine if above unsuitable or not tolerated

32
Q

What is the second line treatment in absence seizures?

A

2nd line - Clobazam, clonazepam, levetiracetam, topiramate or zonisamide

33
Q

What drugs should you avoid in absense seizures?

A

Avoid - carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabaline, tiagabine and vigabatrin.

34
Q

What drugs should you avoid in myoclonic seizures?

A

Avoid - carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabaline, tiagabine and vigabatrin.

35
Q

What is the 1st line treatment in absence seizures?

A

Sodium valproate

Consider levetiracetam or topiramate if sodium valproate unsuitable or not tolerated

36
Q

What is the 1st line treatment in focal/partial seizures?

A

Carbamazepine

lamotrigine

37
Q

What are the adverse effects of antiepileptics?

A

Acute allergic reaction - eg skin rash, Toxic effect - eg unsteadiness, blurred vision, tremor, confusion.

Teratogenicity – eg spina bifida (sodium valproate)

Chronic adverse reactions: Weight gain, weight loss, hair loss, overgrown gums, memory loss, behavioural disturbances, mood changes, anaemia, osteomalacia

38
Q

What are the specific adverse effects of Sodium valproate?

A

Teratogenicity (spina bifida - folate involvement)

Weight gain, tremor, Parkinsonism,

39
Q

What are the specific adverse effects of Carbamazepine, phenytoin, lacosamide and lamotrigine?

A

Tiredness, double vision, unsteadiness

40
Q

What are the specific adverse effects of Topiramate and zonisamide?

A

Weight loss, behavioural changes, paraesthesiae, kidney stones

41
Q

What are the specific adverse effects of Levetiracetam?

A

Tiredness, dizziness, aggression

42
Q

What are the specific adverse effects of Clobazam & clonazepam?

A

Sedation

43
Q

What is the contraception advise given to woman on antiepileptics?

A

If using enzyme-inducing antiepileptic – need COCP containing at least 50µg oestrogen. Using tri-cycle (3 pill packs then 4 days off)

Avoid Implanon implants, POP, patches.

Coil and Depo can be used

44
Q

Which are the anti epileptics that are primarily metabolised by p450 system?

A

Carbamazepine, ethosuximide, oxcarbazepine, phenytoin, phenobarbital, primidone, tiagabine, zonisamide

45
Q

Which drugs are primarily renally excreted?

A

Gabapentin, levetiracetam, vigabatrin, pregabalin

46
Q

When does a seizure become status epilepticus?

A

After 5 mins of a continuous seizure

47
Q

What is the initial treatment of status epilepticus?

A

Community - PR diazepam or buccal midazolam

Hospital - IV lorazepam

48
Q

What do you use to treat serial seizures in status epilepticus?

A

Clobazam

49
Q

When do you give phenytoin in patients with status epilepticus?

A

New patient who has been seizing for 20 - 30 mins

50
Q

Whats the definition of a seizure?

A

A seizure is defined by release of excessive and uncontrolled electrical activity in the brain

51
Q

What are the symptoms of delerium tremens (DT) when will you get it?

A

Acute alcohol withdrawal

Severe agitated confusion:
o Hallucinations, confusion, delusions, sever agitation, GENERALISED TONIC-CLONIC SEIZURES

52
Q

What is the pharmacological treatment of DT?

A

Chlordiazepoxide PO

53
Q

How do you treat wernicke’s encephalopathy?

A

thiamine IV

54
Q

What is the metabolism of phenytoin?

And its subsequent relevance to dosing?

A

Metabolism is dose dependent
• 1st order kinetics initially – as dose increases, metabolism increases at a proportional rate. (Fixed PERCENTAGE of drug metabolized during a per unit time)

At a certain point it undergoes 0 order kinetics (fixed AMOUNT of drug metabolized per unit time – rate is independent of the concentration of the reactants). This is due to saturation kinetics.
• Enzymes are used up, so extra dose wont be metabolised as quickly as its administered.
• Enzyme activity can be enhanced or competitively inhibited by drugs that share the same hepatic enzyme

55
Q

What is phenytoin’s effect on the p450 system?

A

Phenytoin is an inducer of cytochrome P450 enzymes

56
Q

What is the most appropriate drug in generalised seizures?

A

Sodium valproate

57
Q

What is sodium valproate’s effect on the P450 system?

A

Sodium valproate is an inhibitor of cytochrome P450 enzymes

58
Q

What is the key counselling you need to give patients with newly diagnosed epilepsy?

A

Driving, Dangerous situations, Pregnancy and teratogenicity, Interactions of AEDs esp with OCP

59
Q

What is the acute management of generalised seizures?

A

ABCDE - extra attention to patients airway, try to gain IV access
• Oxygen – to prevent hypoxia
• Safe environment – clear surroundings
• Keep patient supported during seizure protecting from injury. As soon as movements cease put into recovery position and ensure she is watched until she has recovered consciousness
• Drug treatment considered after 5 mins (status epilepticus

60
Q

Drugs in status epilepticus

What is the drug class of lorazepam?

A

o Lorazepam
• Benzodiazepine: enhances effect of GABA
• Low lipid solubility

61
Q

Drugs in status epilepticus

What is the route of administration of diazepam and when shouldnt it be used?

A 
Diazepam
•	Can be given rectally
•	Not suitable for IV use >>> thrombophlebitis
•	High lipid solubility
•	CAUTION – Respiratory depression
62
Q

Drugs in status epilepticus

What is the route of administration of Midazolam
and when shouldnt it be used?

A 
Midazolam
•	If facilities for resuscitation not available
•	Given intranasally/buccally
•	Unlicensed use
•	CAUTION – Respiratory depression
63
Q

Drugs in status epilepticus

What is the route of administration of Phenytoin Sodium
and how should you keep an eye on potential ADRs?

A

Phenytoin Sodium
• Slow IV injection
• ECG monitoring
• CAUTION – Bradykinesia, Hypotension

64
Q

What is the main drug in partial seizures?

A

Carbamazepine

65
Q

What is Carbamazepine’s effect on the P450 system & therefore how will it effect warfarin?

A

Enzyme inducer
• Drug interaction with warfarin
• If carbamazepine used, need more frequent INR monitoring for 4-6 weeks

(INR will fall, therefore increased stroke risk)

66
Q

What are the side effects of carbamazepine?

A

Drowsiness, Rash (4-6 weeks), Hyponatraemia (SIADH) & Neutropenia

67
Q

What are the effects of carbamazepine in OD?

A

Carbamazepine causes cerebellar toxicity in OD.

Nystagmus, Ataxia (falls risk), Increased seizure frequency

68
Q

What are the clues that a patients parkinsonism is drug induced?

A
  • Subacute bilateral onset
  • Progression of symptoms concurrent with medication intake
  • Early presence of postural tremor
69
Q

What are some of the high risk drugs that can cause parkinsonism?

A

Dopamine antagonists – Neuroleptics e.g…

HALOPERIDOL & RISPERIDONE

Anti-emetics e.g metoclopramide.

others = Valproate, Lithium, CCBs, SSRIs (fluoxetine)

70
Q

What is the surgical treatment of PD?

What are the advantages & disadvantages?

A

Deep brain stimulation of subthalamic nucleus
• Improves motor fluctuations
• Improves PD features and may permit drug dose reduction
• Does not improve axial problems
• May worsen speech

4TH YEAR - CPTP (19 decks)

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