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Clinical Pharmacology Year V NIŠ > PD, MS > Flashcards

PD, MS Flashcards

1
Q

What is the role of non-ergots?

A
  • non ergots such as Pramipexole or Ropinirole
  • Direct Dopamine receptor agonist
  • Treatment of patients <65 years with Parkinson symptoms without cognitive impairment
  • Specifically presenting with bradykinesia
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2
Q

Side effects of dopamine agonists?

A
  • Non ergots e.g. pramipexole and ropinirole
  • Drowsiness, nausea, orthostatic hypotension, hallucinations
  • Long term use, male sex, high doses also increase chances of compulsive gambling
  • Due to reduced neuronal activity in areas of brain response for impulse and inhibitory control
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3
Q

What COMT inhibitors are used in PD?

A
  • Centrally acting: Tolcapone
  • Peripherally acting: Entacapone
    *Tolcapone has risks of hepatotoxicity
  • Should always be used in combination of of L-DOPA and Carbidopa
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4
Q

What are the main drugs used in PD treatment?

A
  • Dopamine precursor; Levodopa
  • Dopa Decarboxylase Inhibitors; Carbidopa
  • COMT inhibitors
  • MAO Inhibitors
  • Anticholinergics
  • Dopamine agonists (ergot or non-ergot)
  • NMDA antagonist
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5
Q

The risk of which adverse effects are reduced when carbidopa is prescribed alongside Levodopa?

A
  • Orthostatic hypotension
  • Nausea & Vomiting
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6
Q

What is the MOA of amantadine?

A
  • Increase Dopamine release and inhibits uptake
  • NMDA antagonist
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7
Q

What are the adverse effects of Amantadine?

A

-Livedo Reticularis (lower extremity purple rash)
- Ankle edema
- Orthostatic hypotension
- Ataxia
- Prolonged QT interval
- Anticholinergic effects: dry mouth and constipation

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8
Q

What is the MOA of MAO-B inhibitors?

A
  • Inhibit the breakdown of dopamine
  • Increases availability of dopamine
    -E.g. selegiline, Rasagiline
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9
Q

What anticholinergic drugs are used for PD and what are their indications?

A
  • Trihexyphenidol
  • Benztropine
  • Biperidine
  • Patients < 65 years of age with main symptom of ONLY TREMOR
  • Does not treat bradykinesia
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10
Q

What drugs are ergots and non-ergots? What are their indications?

A

-Ergots: Bromocriptine
-Non- ergot: Pramipexole, Ropinirole, Apomorphine
- Ergots no longer recommended for PD therapy due to increased risk of Pulmonary, Cardiac and Peritoneal Fibrosis
- Indicated in early stages of PD, especially < 65 years
- Can be used at any age with used in adjunctive therapy

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11
Q

What is parkinson’s disease

A
  • Neurodegenerative Disorder
  • Affecting dopaminergic neurons in substantia nigra
  • Cardinal signs include: rigidity, bradykinesia or akinesia, postural instability and resting tremor
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12
Q

What is Multiple Sclerosis?

A
  • Chronic demyelinating degenerative disease of the CNS
  • Demyelination and axonal degeneration in the brain and spinal cord
  • Caused by an immune-mediated inflammatory process
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13
Q

What drug is given as first line management (MS) ?

A
  • Corticosteroids
  • Methyprednisolone (PO or IV) or prednisone (PO)
  • 3 to 7 days
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14
Q

What are disease-modifying drugs?

A
  • Medication for long term treatment of MS to prevent relapses
  • These include: glatiramer Acetate, Interferon beta, monoclonal antibodies e.g. natalizumab, dimethyl fumarate
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15
Q

What is the MOA of interferon beta in MS treatment?

A
  • Decrease T cell activation to decrease cytokine secretion
  • Limits T cell access into CNS whilst maintaining integrity of BBB
  • Decreases inflammation (Th2 > Th1)
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16
Q

What are the adverse effects of Interferon Beta Therapy?

A
  • Flu like symptoms: fever, fatigue, myalgia, malaise etc
  • Injection site reaction
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17
Q

What is the MOA of Glatiramer Acetate (Copaxone)?

A
  • Activates Th2 cells to reduce inflammatory processes
  • Acts as a “decoy” for T cells instead of myelin- structurally similar to myelin
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18
Q

What are the side effects of Glatiramer Acetate?

A
  • Injection site reaction
  • Chest pain or palpitations
  • Flushing
  • Anxiety
  • SOB
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19
Q

What is the MOA of Teriflunomide?

A
  • Inhibits synthesis of pyrimidines
  • Cytostatic effect on rapidly dividing B and T cells by inhibiting dihydro-orotate dehydrogenase
  • Therefore causes anti-inflammatory reactions and proliferative processes
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20
Q

What are the side effects of teriflunomide?

A

Side effects: Nausea, diarrhea, alopecia, teratogenicity, headache

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21
Q

What is the MOA of Dimethyl Fumarate?

A
  • An immunomodulator: protects nerve cells through its anti-inflammatory effect
  • shift cytokine production from pro-inflammatory to anti-inflammatory
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22
Q

What are the side effects of Dimethyl fumarate?

A
  • GI disturbances: nausea, diarrhea
  • Headache
  • Liver dysfunction
  • Immunosuppression
  • flushing
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23
Q

What is the MOA of Fingolimode?

A
  • Agonists of the sphingosine 1-phosphate receptor
  • Decrease lymphocyte invasion of the CNS through sequestration of lymphocytes in the lymph nodes
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24
Q

What are the adverse effects of Fingolimode?

A

-Bradycardia
-Liver dysfunction
-Hypertension
-Macular edema
-Headache
-Infections

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25
Q

When is Fingolimode contraindicated?

A
  • MI, HF, TIA, Prolongued QT Interval, AV block
  • Anti-arrhythmic classes Ia and III
26
Q

What is Natalizumab and its MOA?

A
  • Monoclonal antibiotic
  • An antibody against α4-integrin; inhibits lymphocyte invasion of the CNS
  • Inhibits inflammation
27
Q

What are the side effects of Natalizumab?

A
  • Hypersensitivity: itchiness, fever, rash
  • Hypotension
  • Chest pain
  • SOB
  • headache
  • dizziness
  • nausea
  • sweating
28
Q

What is the MOA of mitoxantrone?

A
  • Used for MS treatment
    -strong non selective immunosuppressant
  • inhibition of DNA and RNA synthesis- prevents synthesis of T cells, B cells and macrophages
  • Apoptosis of T cells and APCs preventing T cell activation
29
Q

What are the adverse effects of Mitoxantrone?

A
  • cardiotoxicity
  • Nausea
  • Alopecia
  • Bone marrow suppression
  • Infection
30
Q

What are the indications for Mitoxantrone?

A
  • Secondary MS
  • Progressive MS
  • Progressive- relapsing MS
  • Worsening relapsing-remitting MS
  • reserved for patients with rapidly advancing disease- failed with other therapy
31
Q

What is Alemtuzumab and it’s MOA?

A
  • monoclonal antibiotic
  • Antagonist of superficial antigen CD52; found on the surface of lymphocytes and monocytes
  • Depletes B and T lymphocyte
32
Q

When is alemtuzumab indicated?

A
  • 2nd or 3rd line patient without response to 1st line drugs
33
Q

What are the adverse effects of alemtuzumab?

A
  • Rash
  • Headache, fatigue
  • Infusion reactions
  • Infections
  • Autoimmune phenomena (e.g., ITP, glomerulonephritis, thyroid abnormalities)
  • Malignancies
34
Q

What is Ocrelizumab?

A
  • Monoclonal antibiotics
  • Antibodies against CD20; deplete B cells
  • Humanized anti-CD20
  • 1st drug registered for progressive MS
35
Q

What are the side effects of Ocrelizumab?

A
  • Injection site reactions
  • Infections
  • Hepatitis B virus reactivation
  • URTI
  • HPV infections
  • Malignancies
36
Q

What is the MOA of Cladibrine?

A
  • Synthetic analogue of deoxyadenosine
  • Analog of purine that interferes with DNA synthesis and repair, triggering apoptosis and subsequent lymphocyte depletion
37
Q

What are the side effects of Cladibrine?

A
  • URTI
  • Headache
  • Nausea
    -Leukopenia
  • Infections
38
Q

What is a stroke and its types?

A
  • acute neurological condition caused by abrupt disruption to cerebral perfusion
  • Ischaemic (most common- 80%) and hemorrhagic
  • Neurological deficit last > 24 hours
39
Q

What are the symptoms of a stroke patient?

A
  • weakness of one side of body- unable to raise arms
  • inability to speak- slurred speech
  • Loss of vision
  • Vertigo
  • Unsymmetrical face/smile
40
Q

What is a TIA?

A
  • Transient ischemic attack (TIA) is a temporary, focal cerebral ischemic event that results in reversible neurological symptoms but is not associated with a visible acute infarct on neuroimaging
  • Neurological deficit lasting < 1 hour typically (24 hours by definition)
41
Q

What are some risk factors of stroke?

A

Non-modifiable:
- Age > 55 years
- Male > Female
- Low birth weight
- Specific race

Modifiable:
- Hypertension
- AF
- Cardiac disease: mitral stenosis, Left atrial enlargment
- Diabetes
- Oral contraceptive
- Postmenopausal hormone therapy
- Lifestyle factors: obesity, smoking etc

42
Q

What are primary prevention protocols for Stroke?

A
  • Lifestyle changes
  • Control risk factors:
    maintain BP, glucose levels,
  • Aspirin at low doses (100mg) has anti-platelet effect
  • Aspirin in females > 45 years without increased risk of CNS bleeding
  • Aspirin in females > 65 years with hyperlipidemia, DM
  • Aspirin not effective in Males
  • May increase risk of subarachnoid bleeding
43
Q

What are the secondary prevention protocols for Stroke?

A
  • Lifestyle changes
  • Risk factor control
  • Statins: Arvostatin 80mg
  • Low HDL: niacine, gemfibrozil
  • PCSK9 Inhibitors (e.g. Alirocumab) in combination with statins for high risk patients
  • NO hormone replacement therapy
  • dual antiplatelet therapy after CVI
44
Q

What are the overall goals of stroke management?

A
  • Correct Dx
  • Revascularization via surgery
  • Long term prevention of re-occlusion
  • Decrease risk of TIA/ CVI
45
Q

What are hyper-acute phase management of stroke?

A
  • Oxygen supply
  • Body temperature control
  • Fluid electrolyte balance
  • Glycemia control
  • BP control
  • Control of cerebral edema
46
Q

What fibrinolytic therapy is used for Stroke?

A
  • Alteplase (IV or intra-arterial)
  • Within < 6 hours of symptoms onset
  • Check inclusion & exclusion criteria

e.g. exclude in pregnancy or major trauma/surgery in last 14 days

Include if patient is < 18 age, Dx of ischemic stroke with symptom onset less than 4.5 hours before treatment would begin

47
Q

What is the management plan for ischaemic stroke?

A
  • Thrombolytic therapy (e.g. alteplase)
  • NO anticoagulant or antiplatelets of 24 hrs of thrombolysis
  • Aspirin after 24 hrs, within 48 hours (325mg/day)
  • if BP> 185/105mmHg: antihypertensive
  • paracetamol for pain management (every 4-6 hours)
  • Statins within 48 hours
48
Q

What is the management of intracerebral bleeding- CVI?

A
  • Normalise BP: SBP < 140mmHg
  • CAUSED BY ANTICOAGULATION?- FFP or prohrombin complex, Vit K
    -CAUSED BY ANTIPLATELET?- supportive therapy
  • Hydrocephalus and hematoma: surgical intervention
  • reduce glycemia
  • control body temp
  • hydration
  • anti-epileptics for any convulsions
  • prophylaxis of DVT
49
Q

What is epilepsy?

A
  • a chronic neurologic disorder characterized by a predisposition to seizures as defined by one of the following:
  • Two or more unprovoked or reflex seizures separated by more than 24 hours
  • One unprovoked or reflex seizure in an individual with a high risk of subsequent seizures (e.g., after traumatic brain injury, stroke, CNS infections)
50
Q

Epileptic seizures can be focal or generalised. Explain.

A

Focal: restricted to almost always 1 hemisphere w/o LOC with altered consciousness

Generalised: LOC, both hemispheres and can be tonic, clinic, tonic-clonic, myoclonic, atonic and absence

51
Q

What are the treatment goals of epilepsy?

A
  • the tolerable balance between reduced seizure severity and/frequency and medication adverse effects
  • ease patient QOL
52
Q

What are the antiepileptics used?

A

1st Generation:
Valproic acid, Carbamazepine, Ethosuximide, Phenytoin, Benzo’s, Phenobarbitals

2nd Generation:
Lamotrigine, Topiramate, Gabapentin, Pregabalin, Tiagabine

(and many more 1st and 2nd generations)

53
Q

When should you change the drug?

A
  • inefficient therapy
  • add 2nd drug, gradually decrease the 1st
  • higher success rate if 2nd drug has different MOA to 1st drug
54
Q

When can you use adjunct therapy for epilepsy?

A
  • no success after 2nd drug
  • add a drug with different or complimentary MOA
  • one with max efficiency and one with max safety
  • slow titration
55
Q

When can therapy be ended and when not?

A

Pro:
- no seizures 2-4 yrs
- normal neurological findings and EEG
- full control of seizures in 1 year

Contra:
- Hx of frequent seizures
- repeated episodes of status epilepticus
- a combination of seizure types
- altered mental function

56
Q

What are the common adverse effects of antiepileptics?

A
  • Broad symptoms: sedation, dizziness, diplopia/blurred vision, impaired concentration and ataxia

Concentration specific: sedation, ataxia and diplopia

Idiosyncratic AE: rashes (progression into Steven Johnson Syndrome), hepatotoxicity, hepatotoxicity
*periodic lab testing, especially if emerging symptoms are related

Chronic AE: osteomalacia, osteoporosis, peripheral neuropathy, cerebral atrophy

*serious AE need discontinuation

57
Q

What is status epilepticus (SE)?

A
  • Neurological emergency which may lead to permanent brain damage or death
  • continuous seizures lasting > 5mins or > 2 seizures w/o complete recovery of consciousness
  • decompensation with brain hypoperfusion and brain damage
  • mostly in patients w/o epilepsy
58
Q

How is non-convulsive SE managed?

A

1st line: Benzo’s and/or valproic acid

2nd line: general anaesthesia
- possible to try before anaesthesia with phenytoin or levetiracetam

59
Q

How is convulsive SE managed according to its stages?

A

Developing (0-30 mins): Midazolam

Established (30-60 mins): Phenytoin, valproic acid etc

Refractory (> 2 hours): midazolam, pentobarbitone/thiopentone or propofol, sometimes ketamine

Super-refractory (> 24 hours): ketamine, hypothermia, lidocaine, general anaesthesia for over 24 hours

60
Q

What are the MOA of antiepleptics?

A

Blocking VGNa Channels: reduce Na entry into neurons- Carbamazepine, Phenytoin etc

Block VGCC: lamotrigine and topiramate (can also block NMDA Rs)
Low voltage T-type CCBs: Valproic acid and Zonisamide

Inhibition of high voltage Ca Channel:

Clinical Pharmacology Year V NIŠ (9 decks)

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