Problem Based Learning

Problem based learning (PBL) is a popular method of learning, currently used by most health professional courses in the UK.

The aim of PBL is for you to read through a complex and broad series of information, to identify areas of interest and areas you would like to explore further, in order to further your knowledge of specific topics, through self-directed learning.

 The questions our mentors have provided offer ideas of topics to explore and are written in three streams for aspiring medics, dentists and veterinarians; focus on all three or simply what interests you!

  • Remeber you can leave a comment if you have any questions and we will be sure to answer them.
  • We will  be discussing and answering the PBL cases in the VMS meeting at 7pm – 8pm on 9th March 2020.

Nerve Disorders

THE Dental PBL Case

Background:

Many medical conditions and diseases can influence oral health, as well as, the medications used to treat them. 

 

Scenario

Mrs Jones, a 50 year old woman presents to you for a new patient examination. Mrs Jones is in a wheel chair and was unable to fill out the medical history sheet herself in the waiting room. During verbal history taking, the following medical history was found:

  • She was diagnosed with Relapsing-Remitting Multiple Sclerosis (MS) at the age of 30 years old
  • She takes 15mg of Baclofen 3 times a day
  • She takes 5-day courses of steroid tablets when MS relapses occur

Questions 

  1. What are nerves? 
  2. What type of nerves are there? 
  3. How do nerves work?
  4. What nerves supply:
  • Motor innervation to the muscles involved in chewing?
  • Sensory innervation to teeth?
  • Taste to the tongue?
  • Motor innervation to the tongue?
  1. What is MS?
  2. How might MS affect the nerves of the face and oral cavity?
  3. What is the likely reason Mrs Jones is taking Baclofen and how might this condition affect her oral health? 
  4. What oral side effects might Mrs Jones experience from Baclofen? 
  5. What oral diseases is Mrs Jones likely to be at an increased risk of and why? 
  6. How else might MS affect the oral cavity and how might some of these be treated/overcome?
  7. How might other neurological diseases affect oral health and how might some of these be treated/overcome?

Challenge: 

  1. What barriers might there be for people with neurological conditions accessing dental care and how might these be overcome?

THE Medic PBL Case

Angela is a 60-year-old woman who lives with her husband and dog in a semi-detached house. One Saturday morning, as she was sitting down for breakfast, she noticed that she could not lift her spoon properly with her right arm. She thought this was very strange and that she must have been lying on it earlier when she was reading in bed that morning. She did not think anything more of it until she knocked her coffee mug over onto the floor of the kitchen, which smashed. Her husband heard the noise and came to help her, and he noticed that Angela was slurring her speech. 

 He was very concerned and called an ambulance for her, and Angela was taken to hospital. The junior doctor in the emergency department examined her. They conducted a full neurological examination involving the cranial nerves and the upper and lower limbs. They found that Angela had significantly increased tone, brisk reflexes and decreased power on her right-hand side, with her arm weaker than her leg. There was no significant facial weakness, but she had altered sensation on the right-hand side of her body and homonymous hemianopia (tunnel vision). The doctor noted that her symptoms had come on rapidly 60 minutes ago from taking Angela’s history. 

Angela was sent for an urgent CT scan of her brain, which came back normal. An ECG was performed, which showed atrial fibrillation. She was given some alteplase and admitted to one of the wards for observation and rehabilitation. 

  1. What is the most likely diagnosis for Angela? 
  2. What rapid screening tool can be used in the community to help flag this condition? 
  3. What are the risk factors for this condition? 
  4. What are the two main types of this condition?
  5. Why did the doctor do a CT scan, and what was the significance of the negative findings?
  6. What is the significance of Angela’s newly diagnosed atrial fibrillation?
  7. Why was Angela given alteplase? 
  8. What is Angela’s assessment using the Bamford classification, and why do we care?
  9. What are the different lobes of the brain, and what do they each do?
  10. Challenge: Using the motor homunculus and cerebral artery territories, an infarct involving which artery (and on which side) is likely to have caused her symptoms? (See appendix for additional resources)
  11. Challenge: What would have changed in the doctor’s management had they found that Angela had woken up with her symptoms? Why? 

Cerebral artery territories

Source: Wikipedia 

Motor homunculus

Source: Wikibooks

Main areas of the brain

Source: Frontiersin.org 

 

THE Vet PBL Case

Case 1:

A concerned farmer phones you regarding 3 sheep in his flock which are acting strange since the start of February. He’s noticed them off their feed, disorientated and sometimes running into corners or fences.

Case 2:

Imagine you are a small animal vet dealing with a complicated medical case. Rusty is a 6yo, MN Golden Retriever who used to love walks but now the owners report that after very short walks Rusty is extremely fatigued and weak. His weakness is in all 4 limbs and once he rests it seems to pass until he tries to perform exercise again.

You saw Rusty last week and gave him pain-killers as you thought it may be arthritis but the owner reports no improvement. The owner says Rusty is now retching his food up immediately after eating, they are very concerned about Rusty.

Case 3:

Last month we discussed that horses are hind-gut fermenters. In animals, and humans, the enteric nervous system supplies the gastrointestinal tract with nervous function.

Case 1:

  • What possible diseases could these sheep be suffering from?
  • What further questions would you like to ask the farmer as part of your clinical history?

Case 2:

  • Explain what occurs at the neuromuscular junction.
  • What neuro-muscular disease might Rusty have?
  • How would you test for this disease?
  • What is Rusty’s prognosis moving forward?

Case 3:

  • What category of nervous system does the enteric system come under?
  • What are the clinical signs of Equine Grass Sickness/equine dysautonomia?
  • What are some of the theorised causes of Equine Grass Sickness?
  • Is EGS treatable?

 

 Answers:

What possible diseases could these sheep be suffering from?

Differential diagnoses:

  • Twin lamb disease (Pregnancy toxaemia) in heavily pregnant ewes during the last four weeks of pregnancy.
  • Middle ear infections
  • Brain abscesses
  • Gid (coenurosis, tapeworm cyst taeniea in the brain causing staggering gait/ataxia)

 

What further questions would you like to ask the farmer as part of your clinical history?

What are the sheep grazing/fed on? Has the silage quality been tested? Any mineral deficiencies or toxicities? Has the soil been tested? Have they been moved recently? Has the farmer used any treatments on them? Are there any new members to the flock?

 

Rob to mention this info for first question after students have discussed:

The farmer mentions his silage this year has been poor quality and measures as being less acidic as he would like. You suspect the sheep are suffering from Listeriosis. How does the bacterium make its way to the brain to cause the clinical signs produced (encephalitis)?

  • L. monocytogenes gets ingested and ascends up the trigeminal nerve (possible via the facial nerve or maxillary/mandibular nerves, any branch that terminates in the oral cavity of the sheep)

 

Neuromuscular junction:

  • This is where the end of a motor neuron sends signals to a muscle fibre, ultimately leading to muscle contraction. 
  • A traveling nerve impulse releases acetylycholine (neurotransmitter) at the axon terminal of the motor neuron
  • Ach then crosses the neuromuscular junction and binds to receptor sites on the muscle fiber
  • Acetylcholinesterase (enzyme) destroys ACh molecules so unwanted/prolonged contractions don’t arrise

 

Rusty’s clinical signs are highly suggestive of Acquired Myasthenia Gravis 

  • Disorder of neuromuscular transmission in which muscle weakness results from an autoantibody mediated depletion of acetylcholine receptors (AChR) at the neuromuscular junction.

 

 There are 2 methods of testing for acquired myasthenia gravis in dogs

  • Blood test for ACh receptor antibodies
  • Tensilon test uses edrophonium which is an anticholinesterase drug so it inactivates the acetylcholinesterase enzyme, so ACh can’t be broken down and therefore can accumulate get through the neuromuscular junction and transmit a nerve impulse, this makes more ACh available to the receptors and overpowers the ACh receptor antibodies

 

Rusty’s prognosis moving forward:

  • For dogs who do not experience severe aspiration pneumonia or weakness of the throat and difficulty swallowing, the prognosis is good for complete recovery within 6-8 months.
  • Treatments in dogs usually involve pyridostigmine (delays the breakdown of ACh when it is released from nerve endings) and immunosuppressive therapy

 

 

What category nervous system does the enteric nervous system come under?

  • Autonomic nervous system (involuntary control of glands, smooth muscle, cardiac)

 

 

Grass sickness clinical signs:

  • Dry nostrils
  • Colic signs (rolling, kicking at abdomen, flank watching) but NO GUT SOUNDS
  • Distended stomach (due to poor emptying) —– gastric reflux
  • Tachycardia
  • Muscle tremors
  • Hypersalivation 
  • Dysphagia (difficulty swallowing)
  • Patchy sweating
  • Ptosis (drooped eyelids)

 

Theorised causes of grass sickness:

  • The currently favoured theory under investigation is the possible involvement of Clostridium botulinum type C, a soil-associated bacterium.
  • Many pre-disposing factors come in to play however (location, grazing, field, age)

 

Is EGS treatable?

  • There are acute (PTS), subacute (PTS) and chronic forms of EGS
  • The chronic form is the only type where 50% may be nursed back to health but this is only if their clinical signs fit certain treatment criteria (not in too much colic pain, can still eat, still have a QOL)

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