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Tag: muscular system

How can a weight-loss drug fight sleep apnea?

Teachable moment in classrooms:

  1. respiratory system chapter – anatomy of the upper airways
  2. muscular system chapter – anatomy of the muscles of the tongue and pharynx
  3. nervous system chapter – location of satiety center in the hypothalamus

The news item:  Recently the following report appeared online:

FDA approves weight loss drug Zepbound for sleep apnea

Zepbound, Eli Lilly’s weight loss drug, can now be used to treat obstructive sleep apnea in adults with obesity, the FDA said.

The report states that 39 million adults with obesity in the USA might benefit from this drug treatment. Studies showed that Zepbound significantly reduced the obstruction events in patients. The article also provides a brief description of apnea events, and alternative treatment methods of sleep apnea.

So, Why Do I Care??  Sleep apnea, or more precisely, obstructive sleep apnea, is a sleep disorder that affects millions of adults in the US who suffer from obesity.  Those people are not just losing sleep, but are at higher risk for several cardiovascular diseases, and for daytime sleepiness.  While there are limitations (such as side effects) to the wide use of this drug treatment, it adds to the list of possible treatment options physicians can subscribe.

Plain English, Please!!!   First, let’s talk about sleep apnea.  Apnea is a brief closure of the airways where the closure stops air from getting into the lungs.  The lower portion of our airways have solid cartilage framework (trachea, bronchi), so narrowing rarely occurs; it is always open, like a steel pipe.  However, in the upper airways (mouth, soft palate) we have muscles that surround those airways, and the inappropriate relaxation of the muscles can lead to closure of the upper airway; imagine putting on a sock: it’s easy when we open it up with our fingers, but it’s harder to put our toes through it when the sock is collapsed on the floor. The loss of oxygen flow awakens the person, and repeated instances of apnea leads to poor quality sleep.

Second, let’s talk about throat muscles.  Skeletal muscles in the throat (anatomically called pharynx) and in the soft palate (by specific names: the tensor palatini, levator palatini muscles), and in the tongue

How could we possibly slow down the weakening of skeletal muscles in myasthenia gravis ?

Teachable moment in classrooms:

  1. muscle tissue chapter – structural components of the neuromuscular junction
  2. muscle tissue chapter – role of acetylcholine receptor in muscle excitation
  3. immune system chapter – components and function of complement system

The news item:  Recently the following news item appeared online:

FDA approves drug for adults with generalized myasthenia gravis

AstraZeneca has announced FDA approval of Ultomiris, a long-acting C5 complement inhibitor for the treatment of adults with generalized myasthenia gravis. According to a company press release, Ultomiris (ravulizumab-cwvz) was approved for adult patients who are anti-acetylcholine receptor antibody-positive, which represents 80% of people with the disease.

The article states that the disease myasthenia gravis affects about 90,000 people in the US, and that Ultomiris is a long-acting C5 inhibitor that allows early treatment leading to lesser amount of damage.

So, Why Do I Care??  The article’s citation of the number of affected individuals shows that this is not a minor disease. In its advanced stage myasthenia gravis can be deadly, or at least life threatening; the loss of muscle strength prevents the patients from many daily activities, which causes a decreased quality of life.

Plain English, Please!!!  First, let’s talk about what myasthenia gravis is. Myasthenia gravis is an autoimmune disorder where the patient’s own immune system attacks and damages the neuromuscular junction. The target of the immune system is a molecule, the acetylcholine receptor, in the neuromuscular junction. The acetylcholine receptor physically binds to the messenger molecule called acetylcholine released by the neurons. So, destruction of the receptor makes it impossible for skeletal muscles to understand that they are supposed to contract. The damaged muscles no longer contract with normal force, thus the patients develop muscle weakness that affects movement, and can endanger inhalation causing respiratory distress.

Second, let’s talk about how myasthenia gravis causes damage. The first action of the immune system in myasthenia gravis is to make antibodies that stick to the acetylcholine receptors. The second action is that the antibodies in the neuromuscular junction attract the proteins of the complement system. The 9 complement proteins stick to each other, assemble on the cell membrane, and eventually open a hole in the muscle cell membrane. Imagine an excavation crew where all 9 members have to work together to dig a hole. Those holes in the muscle cell membrane cause the most significant damage to the neuromuscular junction.

Third, let’s talk about how Ultomiris works. The active ingredient in Ultomiris covers up a complement protein (#5), and prevents the piling up the rest of the complement proteins. Without the assembly of all of those proteins the excavation crew never starts to dig, the hole never forms in the muscle cell membrane, and the neuromuscular junction can stay relatively undamaged. That kind of protection slows deterioration, and preserve muscle strength in the patients.

 

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What is the anatomy and physiology behind Justin Bieber’s facial paralysis?

TeachableMedicalNews article 07252022

Teachable moment in classrooms:

  1. skeletal muscle chapter –functioning of skeletal muscles depend on neuromuscular junction
  2. brain anatomy chapter – anatomy and function of cranial nerve VII
  3. muscular system chapter – actions of muscles of facial expression
  4. microbiology – viruses need to enter human cells

The news item:  A news report appeared recently:

Justin Bieber’s wife Hailey gives update after Ramsay Hunt syndrome diagnosis: ‘Getting better every day’

Justin Bieber has canceled several tour dates due to his Ramsay Hunt syndrome diagnosis. Here’s what we know about his recovery, concert plans.

The article stated that Justin Bieber is suffering from type II Ramsay-Hunt syndrome. This is caused by an activation of the Herpes Zoster virus (causes the disease called shingles) that causes paralysis of the facial muscles, and prevents blinking or smiling on one side of the face.

So, Why Do I Care  While it is true that facial paralysis is not a deadly disorder (and only 0.5% of shingles patients develop it), but understanding how it comes about can be useful.  Because facial paralysis gives unusual changes to one’s facial expressions, the symptom is highly visible.  That highly visible nature makes facial paralysis an early warning sign of strokes or trauma to cranial nerves, disorders that are serious malfunctions of the our nervous system.

Plain English, Please!!!  First, let’s talk about what paralysis is. The loss of movement of body part or parts is defined as paralysis. Body parts are moved by muscles, and muscles must receive nerve signals,

How can Zolgensma gene therapy help children with spinal muscular atrophy?

TeachableMedicalNews article 09302021

Teachable moment in classrooms:

  1. cellular basis of life chapter – role of mRNA in protein synthesis
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. muscular system chapter – role of nerve impulses in directing muscle contraction
  4. nervous system chapter – functions of dendrites and axons of neurons

The news item:  Recently the following reporting was published by BBC news organization:

‘Gene therapy is a game changer for our son’

A five-month-old becomes the first person in England to get a drug with a list price of £1.79m.

The article describes the symptoms, such as loss of mobility in infants, of the spinal muscular atrophy.  The article also mentions the mutant SMN1 gene, and the Zolgensma treatment that replaces the mutated gene. The article states that the frequency of this disorder is 1 in 10,000 births.

So, Why Do I Care??  Most children whose symptoms begin after age 2 have a near normal life expectancy. However, newborns with the “infant-onset” form (about 400 newborns each year) have a very short life expectancy. That is devastating to parents, too, who are helpless while their child lays motionless, and not developing motor skills for movement or speech. Innovative treatments not only raise the hope for a more normal life for the affected infants, but also points to possible treatments of similar disorders.

Plain English, Please!!!  First, let’s talk about what is spinal muscular atrophy (SMA).  This disorder originates from damaged neurons in the spinal cord. The consequence of that damage is that skeletal

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