Brainscape's Knowledge GenomeTM

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


See full index

Clinical Physiology > CVA, Parkinson's, Myasthenia Gravis > Flashcards

CVA, Parkinson's, Myasthenia Gravis Flashcards

1
Q

how does myasthenia gravis develop?

A

antibody binds to - acetylcholine receptor

blocked or destroyed

main neurotransmitter cannot bind to receptor

lack of propagation of signal from motor neuron to muscle cell

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

investigations for myasthenia gravis

A

Abs – Anti-AchR, anti-MUSK, anti-LRP4

Electrophysiology – Repetitive nerve stimulation, single fiber electromyography

Edrophonium test

Check for other autoimmune conditions – TFTs, B12

CT chest – AchR Ab +ve MG strongly associated with thymoma

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

triggers of myasthenia gravis

A
  • physical exertion, infection, surgery, pregnancy, hypokalemia
  • antibiotics
  • CCBS
  • beta blockers
  • diazepam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

treatment for myasthenia gravis

A
  • acetylcholinesterase inhibitor (pyridostigmine) - first line
  • prednisolone
  • steroid sparing agents - azathioprine, mycophenolate mofetil
  • acute deterioration - IVIG, plasma exchange
  • novel monoclonal antibody treatments - rituximab, complement inhibition, anti-fc receptor antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

myasthenia gravis mimics ______

A

lambert eaton myasthenic syndome

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

what is myasthenia gravis

A

autoimmune antibody mediated disease resulting in progressive weakness at the neuromuscular junction

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

key differences between myasthenia gravis and Lambert eaton myasthenic syndrome

A
  1. PATHOPHYSIOLOGY - MG post synaptic ach receptors, LEMS presynaptic calcium channels
  2. EXERTION - MG worsens, LEMS improves
  3. TESTING DIFFERENCES - MG dec amplitude CMAP after 2-3 Hz rep stimulation, LEMS inc amplitude CMAP after 50Hz rep stimulation
  4. SYMPTOMATIC THERAPY - MG acetylcholinesterase inhibitors, LEMS 3,4 diaminopyridine
  5. COMORBID ISSUES - MG thymoma, LEMS sclc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

corticospinal tract (movement tract) path

A

starts at motor cortex
medulla
spinal cord
peripheral nerves to target muscles

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

the motor cortex direct pathway controls _______

A

initiation of voluntary movement

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

the motor cortex indirect pathway controls _______

A

prevention of involuntary movements

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

what is parkinsons disease?

A

neurodegenerative disease which causes a progressive decline in the neurological function and loss of neurons.
the most concentrated loss of neurons is in the ganglia.

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

causes of parkinsons disease

A

sporadic condition - normally no underlying genetic mutations, combination of environmental and common genetic factors

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

pathology of parkinsons disease

A

alpha synuclein becomes sticky and clumps forming lewy bodies in dopaminergic neurons.

these are toxic - they build up into brown neuromelanin - this specifically affects dopaminergic neurons

dopamine gradually dies away due to lewy bodies

inclusions can develop decades before motor symptom onset

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

pathophysiology of parkinsons disease

A

the amount of dopamine in the synapse is regulated
too much or too little makes smooth continuous movement difficult

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

Presenting symptoms of parkinsons

A

tremor
difficulty with fine movements
stiffness of a limb
falls

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

diagnostic symptoms of parkinsons

A

akinesia/bradykinesia
tremor
rigidity
postural instability

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

characteristics of parkinsons akinesia/bradykinesia

A

slow movement and decreased amplitude when repeated
difficulty initiating movement
facial hypomimia
lack of arm swing
finger taps
reduced spontaneous blinking

18
Q

characteristics of parkinsons tremor

A

4-7Hz
initially unilateral
pill rolling
reduces on action

19
Q

characteristics of parkinsons postural instability

A

stooped gait, shuffling steps
falls
cannot stand with arms crossed
positive pull test

20
Q

non motor features of parkinsons

A

neuropsychiatric - depression, anxiety
sleep related problems - daytime sleepiness, vivid dreams
cognitive - dementia
autonomic dysfunction - urinary incontinence, erectile dysfunction, postural hypotension

21
Q

what are parkinsons treatments based on?

A

symptomatic treatment giving dopamine

22
Q

medical treatment for parkinsons

A

L-dopa, levodopa - increases dopamine in brain

dopamine agonists

MAOB inhibitors - inhibits breakdown of dopamine

COMT inhibitors - inhibits breakdown of dopamine

23
Q

side effects of levodopa

A

nausea, vomiting, end of dose dyskinesia, confusion, hallucination, on-off syndrome

24
Q

side effects of dopamine agonists

A

impulse control disorders

25
Q

example of dopamine agonist and its side effects

A

apomorphine
nausea, confusion, low BP

26
Q

example of L-dopa

A

duodopa

27
Q

diagnosis of parkinsons

A

history and examination usually confirm
queen square brain bank diagnostic criteria
DAT scan - differentiate between essential and parkinson tremor

28
Q

potential disease modifying approaches

A
  1. precision approach for mitochondrial parkinsons
  2. precision approach for lysosomal parkinsons
  3. precision approach for LRRK2 parkinsons
  4. broad approach to target alpha synuclein
  5. broad approach to target cell to cell transmission
  6. broad approach for neuronal survival
29
Q

ischemic stroke

A

clot blocks flow to area of the brain

30
Q

haemhorragic stroke

A

burst blood vessel causes bleeding into brain

31
Q

virchows triad

A

blood vessel injury
reduced blood flow
increased coaguability

32
Q

causes of blood vessel injury

A

trauma, surgery, hypertension, invasive procedures

33
Q

causes of reduced blood flow

A

AF, long distance travel, varicose veins, venous obstruction, immobility

34
Q

causes of increased coagulability

A

sepsis, smoking, coagulation disorders, malignancy

35
Q

treatment for stroke 6-12 hrs

A

endovascular thrombectomy

36
Q

treatment for stroke <4.5 hrs

A

potent anticoagulant - otoplase, streptokinase

37
Q

why cant anticoagulant be given more than 4.5 hrs after?

A

risk of fatal bleeding - intercranial, large infarction - brain becomes gel

38
Q

treatment for stroke >12 hrs

A

high dose aspirin
long term clopidogrel
antiplatelets and high dose statins reduce long term risk

39
Q

subarachnoid haemhorragic stroke

A

bleeding on surface of brain increasing pressure

40
Q

types of stroke

A

ischaemic. haemhorragic. subarachnoid haemhorragic

Clinical Physiology (11 decks)

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